Final Flashcards

1
Q

Why is cytomegalovirus dangerous when it comes to organ transplantation

A

It is the number one cause of disease and death in transplant patients

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2
Q

Infection in transplant patients of the cytomegalovirus can lead to what?

A

Pneumonia

It is a common complication of bone marrow transplant patients since disease is due to immune response

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3
Q

What complication does the cytomegalovirus cause in AIDS patients?

A

Blindness

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4
Q

What are the treatment methods for cytomegalovirus (CMV)

A

Ganciclovir

Foscarnet and cidofovir

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5
Q

What kind of virus does the cytomegalovirus have?

A

There is no vaccine

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6
Q

What is the diagnosis for the cytomegalovirus (CMV)

A

Serology for the primary infection
Viral isolation
PCR

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7
Q

Why is viral isolation hard for the cytomegalovirus (CMV)

A

It is the slowest growing herpesvirus so diagnosis takes about two weeks

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8
Q

What are the symptoms of the human herpesvirus 6 (roseola)

A

High fever with a rash for two days

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9
Q

What are the major complications with the herepesvirus 6 (roseola)

A

Encephalitis since it can replicate in the brain

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10
Q

What is the treatment for human herpesvirus 6 (roseola)

A

There is no treatment since rash is usually mild. There is also no vaccine for is as a result

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11
Q

What does the human herpesvirus 7 infect?

A

CD4+ T cells

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12
Q

What latent persistent viruses play a role in tumor formation?

A

Human papilloma virus and gamma herpesvirus

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13
Q

What chronic persistent virus plays a role tumor formation

A

Hepatitis B virus and hepatitis C virus

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14
Q

What is cancer?

A

Abnormal or uncontrolled growth

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15
Q

What is an oncogene

A

A gene that has been mutated given the ability of transformation in the cell, thus leading to abnormal division and growth of the cell

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16
Q

What is a proto-oncogene

A

The normal version of a gene that if mutated has the potential of causing abnormal cell growth and become an oncogene

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17
Q

What is a tumor suppressor

A

A protein that inhibits growth to prevent abnormal growth of the cell

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18
Q

Name the two common tumor suppressors

A

pRB which inhibits progression through the cell cycle (retina blastoma)
P53 which can cause apoptosis of the cell if there is DNA damage

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19
Q

What tumor suppressor mutation is on of the largest seen in human cancer?

A

P53

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20
Q

What is transformed cell

A

A cell that becomes a cancerous one due to some kind of mutation

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21
Q

What are the steps in organisms toward oncogenesis

A

Initiation, promotion, and progression

You generally need a lot of mutations for the cancer to arise

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22
Q

How is oncogenesis promoted in cell culture?

A

Immortalization, then transformation

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23
Q

Can acute viruses cause cancer?

A

Generally, no

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24
Q

What are the two methods that a virus can cause cancer

A

Direct and indirect method

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25
Q

What is the direct way that a virus can cause cancer?

A

By carrying an oncogene that is transcribe with it in the cell

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26
Q

What is the indirect method for viral infection causing cancer

A

Chronic viruses can cause constant death and regeneration of cells that normally do not divide lead to an accumulation of mutations
Retrovirus genome insertion next to an oncogene can alter regulation
Very slow

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27
Q

Why are chronic viruses dangerous

A

Constant death of cells in tissue causes constant regeneration which can lead to an accumulation of mutations in the cells which can lead to too many mutations causing cancer.
Liver is especially dangerous because it has rapid regeneration

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28
Q

What direct viruses encode an oncogene

A

Retrovirus (Roy’s sarcoma virus)
Small DNA virus (HPV, MCPyV, SV40)
Large DNA virus (herpesvirus)

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29
Q

Why do viruses evolve to interact with tumor suppressors

A

Activate cellular machinery so that replication of virus can begin
It will also block programmed cell death so that the virus can survive

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30
Q

How is the papillomavirus maintained in the human

A

As an episome

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31
Q

What does the human papillomavirus cause?

A

Warts

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32
Q

Describe the spread of the human papilloma virus

A

On skin, usually when there are cuts on the fingers, wart can appear
Genital warts are spread sexually

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33
Q

What is the major problem with the human papilloma virus

A

The are a major cause of cervical cancer

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34
Q

What virus is associated with head and neck cancer

A

Human papilloma virus

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35
Q

How would someone get throat cancer?

A

Oral sex, it is made worse by smoking

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36
Q

Describe human papilloma virus replication

A

Virus replicates in the spinous layer on skin (where all early genes are expressed) The no dividing cells where the particles are released in the upper layers (where late genes are expressed)

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37
Q

Where is the human papilloma virus latent

A

In the basal level cells where early early genes are expressed

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38
Q

Describe the treatment for warts

A

Cryosurgery and laser treatment for removal of the wart

You can also use immune activators, salycilic acid treatment

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39
Q

What is salycilic acid treatment

A

Killing the skin in the wart area to kill all of the virus

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40
Q

What is the fourth leading cause of cancer death in women

A

Cervical carcinoma

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41
Q

What external factor exacerbates cervical cancer?

A

Smoking

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42
Q

How does HPV cause cervical cancer?

A

It causes an abnormal expression of E6 And E7 in the basal andsuprabasal layers of the skin leading to abnormal cell growth and ultimately cervical cancer
E6 prevents p53 from working
E7 promotes pRB in the cell in order to increase cell cycle

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43
Q

What is the HPV vaccine

A

Gardasil, it contains a single capsid protein to generate an immune response
This is given to women and girls
Now it can be given to men
Has 4 strains and gardasil 9 has 5 new strains added

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44
Q

What tumor viruses are associated with the gamma herpesvirus?

A

Epstein bar virus (EBV)
KSHV
Herpes Virus saimiri

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45
Q

What kind of virus is the Epstein Barr virus?

A

A gamma herpesvirus

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46
Q

What kind of infection does the Epstein Barr virus establish?

A

Life long latency

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47
Q

What is a major complication with the Epstein Barr virus?

A

Cancer due to its life long latent infection

It also cause infectious mononucleosis

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48
Q

What are the symptoms of mononucleosis?

A

Sever fatigue
Sever lymphadenopathy
Slenemology, lasting about a month

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49
Q

What is responsible for the disease caused by mononucleosis, caused by the Epstein Barr virus?

A

Expansion of Bcells and Tcells

Fatigue could be due to cytokines release

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50
Q

What age group does mononucleosis affect

A

Usually teens but not children

Children are usually a symptomatic

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51
Q

Where is burkeitts lymphoma endemic?

A

Africa, usually in children too

Areas with high malaria rates

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52
Q

What causes burkitts lymphoma

A

Epstein Barr virus in all of African cases, but only for half of the cases in North America

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53
Q

What does burkitts lymphoma require in order to produce the cancer

A

C-myc chromosomal translocation leading to over expression of an oncogene

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54
Q

What diseases does the Epstein Barr virus cause?

A

Burkitts lymphoma
Nasopharyngeal carcinoma
Lymphoproliferative disease

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55
Q

What is nasopharyngeal carcinoma

A

Infection of epithelial cells caused by Epstein Barr virus

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56
Q

Who does the lymphoproliferative virus infect?

A

Usually immunocompramised patients and people with HIV

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57
Q

What cells does the Epstein Barr virus infec (EBV)

A

Epithelial cells and resting B cells in the oral cavity

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58
Q

How does the Epstein bar virus become cancerous?

A

Translocation of the viral genome next to c-myc site that causes An increase in cell proliferation. This usually happens in the epithelial cells and rarely B cells

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59
Q

What kind of infection of the Epstein Barr virus in epithelial cells happens?

A

Latent and lyric infection

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60
Q

What kind of genes does the Epstein Barr virus express to promote oncogenesis?

A

It has 10 genes expresses and of those, LMP1 acts as an oncogene in cultured cells because it prevent s apopotosis

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61
Q

What are the symptoms of EBV

A

Fever, pharyngitis, lymphadenopathy, splenomegly

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62
Q

What is the diagnosis for EBV

A

Look for an increase in the total lymphocytes

Serology, look for heterophilic antibodies and EBV specific antibodies

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63
Q

What is the treatment for EBV

A

Moral support, HSV treatments do not work well

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64
Q

What is kaposi’s sarcoma?

A

Tumor caused by gamma herpesvirus

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65
Q

What is the most common tumor in AIDS patients

A

Kaposi’s sarcoma, a gamma herpesvirus

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66
Q

Where is KS endemic (kaposi’s sarcoma)

A

Sub Saharan Africa

Most common reported tumor overall in some countries

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67
Q

During the latency stage of the herpes simplex virus, what is made?

A

Latency associated transcripts

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68
Q

• Describe the latency associated transcripts of the herpes simplex virus

A

o There is no protein made from this and the t-cells cannot target any protein to create an immune response against the virus
o These are turned into microRNAs

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69
Q

• What is the role of the latency associate transcripts?

A

o It blocks apoptosis of the cell

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70
Q

• What are microRNAs

A

o Small regulatory RNAs

o An example is Latency associated protein

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71
Q

• What is the problem with the immune response targeting the herpes simplex virus?

A

o There are no proteins for the immune system to target allowing the cell to remain in the latent state
o T-cells only respond during the reactivation phase of the virus

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72
Q

• When are t-cells activated against the herpes simplex virus?

A

o When the virus is reactivated but not in the latent state

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73
Q

• Other herpesviruses that are lateen in dividing cells make proteins to maintain the viral genome as an episome when cells divide, why does HSV not need to do this?

A

o Because the herpes simplex virus infect non dividing cell (neurons) therefore there is no need for it to maintain itself during replication

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74
Q

• What is the difference between the lytic and the latent state of the herpes simplex virus

A

o In lytic state, over 80 genes are expressed while in the latent state, only one gene is expressed
o In the lytic state the virus replicates rapidly through the use of the host machinery while in the latent state there is no replication happening because the herpes simplex virus infects non dividing cells (neurons)
o In the lytic state, the infected cell dies while in the latent state, the infected cell is alive until reactivation toward the lytic state
o In the lytic state, the virus cause lesion in the lips and genitals while there is no disease created during the latent state
o In the lytic state, there are antiviral drugs that can inhibit the replication of the herpes simplex virus, while during the latent state, there are no drugs because there is nothing to target
o In the lytic state the immune system will eventually shut down the virus, but in the latent state because there is nothing for the immune cells to target, there is no immune attack on the latent herpes simplex virus

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75
Q

• How is the herpes simplex virus reactivated?

A

o Stress, UV light, fever, hormonal changes, menstruation

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76
Q

• How does the herpes simplex virus reactivate?

A

o Upon activation, the virus will initiate lytic replication inside the neurons. This infection will then travel from the neuron to the original site of the lesion and begin to spread to other cells causing more lesions

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77
Q

• How does the herpes simplex virus affect immunocompromised patients?

A

o The sores upon reactivation become very large and cover most of the skin

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78
Q

How much of the herpes simplex virus gets reactivated during the reactivation stage?

A

Only a small percent

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79
Q

What is a major complication of the herpes simplex virus?

A

Encephalitis, but this is very rare

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80
Q

How can the herpes simplex virus cause encephalitis?

A

Upon reactivation of the virus, the virus can travel in the opposite direction and infect the brain instead where it will then replicate. This leads to encephalitis and ultimately death if untreated

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81
Q

How is the herpes simplex virus diagnosed?

A

You can take skin scraping of the legion and grow the cells in culture in order to isolate the virus
You can also isolate the virus from cerebral spinal fluid in order to detect encephalitis
PCR of spinal fluid (spinal tap)
Check for antibodies in pregnant women to see if the women has had the infection before

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82
Q

What is the treatment for the herpes simplex virus?

A

Antiviral chemotherapy. This is Acyclovir drug

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83
Q

How does Acyclovir work?

A

It is treatment for the herpes simplex virus and it works by phosphorylating the viral thymidine kinase. This will then be incorporated in the DNA chain and the incorporated acyclovir will then terminate the ongoing DNA chain
This only works on the lytic virus
Generally, it blocks the replication cycle of the herpes simplex virus

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84
Q

What is the prevention method for the herpes simplex virus?

A

There are no vaccines for the herpes simplex virus
Use of condoms
Taking Valtrex

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85
Q

Describe the basic principles of the Varicella Zoster Virus (VZV)

A

It is a herpesvirus and it is the cause of chicken pox

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86
Q

What is the major problem with reactivation of VSV?

A

The person can get shingles

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87
Q

Describe shingle

A

Extremely painful reactivation of the third herpes virus. It is a neuronal disease that usually spreads from shoulder to the groin

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88
Q

Can someone get the shingles virus from a primary infection?

A

No

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89
Q

Describe the Varicella Zoster virus infection

A

Same replication cycle as HSV

Initial infection becomes disseminated

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90
Q

What is the major complication with the Varicella Zoster virus?

A

It can also cause encephalitis but like in HSV, this is very rare

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91
Q

Where does the Varicella Zoster virus establish latency?

A

In the neurons of the trigeminal and dorsal root ganglia for life of the host.
Reactivation usually happens only once

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92
Q

What is the most infectious human herpesvirus?

A

Varicella Zoster virus (VSV)

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93
Q

Describe the spread of infection by the Varicella Zoster Virus

A

It is spread through the respiratory route.

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94
Q

Where does the infection of the varicella Zoster (VSV) spread?

A

Infection will begin at the upper respiratory tract where it will the disseminate through the body via the bloodstream

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95
Q

Can shingles be spread?

A

No it can only come up upon reactivation of the latent state of the primary infection of the Varicella Zoster virus

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96
Q

Describe VSV dissemination within the host

A

First the infection begins in the upper respiratory tract where the virus will then replicate in the lymph nodes. Then the virus will spread as primary viremia allowing the virus to replicate in the liver, spleen and other organs. Then the virus will continue as secondary viremia leading to infection of skin and vesicular rash

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97
Q

Describe the diagnosis of VSV

A
Basically you can look at the symptoms since they are very distinct
You can also use lab diagnosis
Elisa for antigen
Culture the virus
In situ hybridization
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98
Q

Describe the treatment for Varicella Zoster virus

A

You can use antibody therapy to make the disease shorter
For high risk cases, you can use Vzig
Acyclovir can also be used

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99
Q

What is the prevention method for VSV?

A

There is a live attenuated vaccine called “Oka” that is given to infants

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100
Q

What are the problems with use of the VSV vaccine?

A

There is a potential danger that the future vaccinated children, when adults can become susceptible to the virus because the long term future is still unknown for the capabilities of the vaccine

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101
Q

Describe the Herpes B virus

A

This is an alpha herpesvirus that is found in Macaque monkeys
This spread to humans through zoonotic infection during handling of monkeys
There was only one case of human to human transmission.

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102
Q

Why is the cytomegalovirus most common on the 2nd child?

A

the first child brings home the virus from school

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103
Q

What virus is the most important cause of congenital viral infection in the US

A

cytamegalovirus (CMV)

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104
Q

How is Cytomegalovirus spread?

A

usually by saliva but can be spread through blood

also breast milk, saliva, sexualy, urine, organ transplant, transplacental barrier

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105
Q

What can happen through prenatal infection of the cytomegalo virus

A

Deafness, brain damage, encephalitis, hepatitis

usually happens in the first trimester

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106
Q

Describe the pathogenesis of the cytomegalovirus

A

It will first infect mucosal epithelial cells where it will spread to leukocyte viremia and infect/establish latentcy in hematapoetic stem cells

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107
Q

What virus is the largest human herpesvirus?

A

cytomegalovirus

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108
Q

What kind of virus is the cytomegalovirus

A

Beta herpesvirus

has slow lytic growth

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109
Q

What is the treatment for parvovirus B19

A

antiinflamatories to prevent arthritis

blood transfusion for anemic patients

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110
Q

What is the diagnosis for parvovirus B19

A

Serelogical assay for IgG

PCR assay

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111
Q

What genes are expressed during the various phases of HSV Gene expression

A

Intermediate early genes-regulatory genes
Early genes-replication genes
Late gene-structural genes

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112
Q

Describe the epidemeology of the parvovirus

A

It has a world wide prevelance and most people actually get this

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113
Q

What is the biggest complication with parvovirus infection of the fetus

A

Miscariage

leads to severe anemia which can cause hydrops fetalis leading to fluid build up in fetus

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114
Q

Why is the parvovirus dangerous for pregnant women

A

It can cross the placental barrier

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115
Q

Why does a rash arise in the parvovirus infection?

A

immune system

at this point the patient is not infectious

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116
Q

What are the symptoms of the Erythema infectiousum

A

Redness in skin
mild rash on cheeks
mild arthritis in adolescents
anemia in immunosuppressed patients

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117
Q

What is it called when the parvovirus infect erythroid lineage cells

A

erythema infectiousum

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118
Q

What cells does the parvovirus infect?

A

erythroid lineage cells of bone marrow that will become red blood cells
fetal liver cells

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119
Q

What does the parvovirus need in order to replicate

A

actively dividing cells

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120
Q

Compared to its adeno associated virus cousin, how is paravovirus B19 different

A

It can replicate on its own

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121
Q

What is the Rubella Diagnosis

A

Use IgM elisa for congenital infection for pregnant mother.
High IgM levels without IgG means further tests must be done on fetus
Virus isolation in cell culture
Rt-PCR

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122
Q

Why is is dangerous to give the rubella vaccine during child bearing years?

A

Possibility of infecting the fetus since IgM cannot cross the placental barrier

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123
Q

Describe the Rubella vaccine

A

Live attenuated vaccine

provides life long protection with little side effects

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124
Q

Describe the epidemiology of congenital Rubella Syndrome

A

Due to vaccine, occurance are rare in the united states
developing countries have lower vaccination rates so the occurances are higher
amish people do not get vaccines so it is more common for them

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125
Q

What can happen to the fetus if the mother has a primary infection of Rubella within the first 16 weeks

A
mental retardation
cataracts
heart defects
premature delivery
deafness
not too common after first trimester
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126
Q

If Rubella is such a small infection, what is the major problem with it?

A

Congenital Rubella syndrom

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127
Q

What is the treatment for rubella

A

No treatment since the infection is usually mild

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128
Q

What is the uncommon symptom of Rubella childhood infection

A

mild encephalitis-headache-vomiting

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129
Q

Describe the childhood pathogenesis of Rubella

A

It first infect through spread by aeresol droplets infectin mucosa of upper respiratory tract
It will then travle by primary viremia to the lymph nodes where it will then spread to secondary viremia, where it will then cause rash from face to feet

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130
Q

What are the three types of mother to child transmissions

A

Intrauterine
Intrapartum
postnatal

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131
Q

What is the word for infection of the fetus during pregnancy

A

Intrauterine

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132
Q

What is the word for infection of the baby during the birthing process?

A

Intrapartum

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133
Q

What is the word for vertical transmission that happens after birth

A

Postnatal

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134
Q

Describe the intrauterin process. What must the virus do to infect the fetus

A

Virus must cross the placental barrier in order to access the fetus or else virus will be filterd out
virus can also ascend from the genital tract

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135
Q

What does the placenta do for the baby

A

separates mother and fetal blood so that it does not mix

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136
Q

What are the cell layers that separate mother and fetal blood? That create the placental barrier

A

Syncytiotrophoblasts
Cytotrophoblasts
basil lamina layer

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137
Q

What antibodies play a role in fetal immunity

A

IgG and IgM

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138
Q

What antibody in fetal immunity can cross the placental filter

A

IgG

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139
Q

What antibody in fetal immunity is too large to cross the placental filter?

A

IgM

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140
Q

Describe the role of IgG in fetal immunity

A

This can cross the placental barrier allowing the mothers antibodies to be passed to the fetus for protection

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141
Q

Describe the role of IgM in fetal immunity

A

It cannot cross the placental barrier because it is too large, therefore, during primary infection, there is no immunity from the mothers antibodies to the fetus

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142
Q

Why is reactivation of HSV in the mother much less dangerous to the neonate than primary infection

A

IgM antibodies are too big to cross the placental barrier, therefore, the virus can infect and cause harm to the fetus

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143
Q

What is the advantage and disadvantage to breast feeding

A

Virus such as HIV can be transmitted

you can get IgA antibodies this way

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144
Q

What are the possible complications with fetal infections

A
Brain damage
mental retardation
development problems
spontaneous abortion
deafness
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145
Q

How do fetal infections of the virus cause defects?

A

The virus will replicat in specific cell types causing destruction of important cells during development

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146
Q

How is HIV verticaly transmitted

A

transmission happems in utero, through blood, genital secretion, and breast milk

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147
Q

Why is HIV through vertical transmission dangerous?

A

The time between HIV to AID is greatly accelerated

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148
Q

What is a major complication of vertical transmission of the herpes simplex virus

A

Brain damage

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149
Q

What are the hosts for the rubella virus

A

human, no known childhood infector

mainly children

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150
Q

What are the symptoms of a rubella childhood infection?

A

Mild rash
low grade fever
lymphadenopathy

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151
Q

What is the drug used for HSV treatment

A

acyclovir

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152
Q

What does Acyclovir for HSV do?

A

blocks herpes simplex from replicating

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153
Q

What does the herpes simplex virus cause in human

A
facial of genital sores
keratitis
encephalitis
herpetic whitlow
disseminated sores in immunocompramised people and neonates
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154
Q

What is keratitis and what virus causes it?

A

eye disease and HSV

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155
Q

What causes herpes simplex lesions?

A

Virus infects muco epithelial cells, spreading cell to cell causing death and inflammation
forms single or multiple lesions that creates a small painful ulcer because it infects the neurons in this region. Virus is then cleared

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156
Q

To cause lesion, what cells do the HSV virus infect?

A

mucoepithelial cells

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157
Q

When a herpes simplex lesion is about to reoccur, what does a person usually experiance

A

a tingling feeling at the initial infection site

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158
Q

How is the herpes simplex virus spread?

A

direct contact through kissing
sexual transmission
finger cuts
vertical transmission

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159
Q

How is the herpes simplex virus spread through kissing

A

Direct contact because is allows HSV to infect the subcutaneous epithelial cells in the lip area

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160
Q

What is it called when a herpesvirus is obtained from finger cuts

A

hepetic whitlow

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161
Q

Describe the vertical transmission of HSV-2

A

The mother can pass to infant if she gets a primary infection. Reactivation usually does not lead to spread because the mother has antibodies to pass on to the child
birth canal with herpes lesions will most likely cause spread leading to brain damage and overall death

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162
Q

Is the herpesvirus usually symptomatic

A

no, asymptomatic

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163
Q

What is the problem with the spread of herpes?

A

most people are asymptomatic, so they can spread the virus without knowing that they actually are

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164
Q

What cells does the HSV infect and describe its pathway toward infection

A

Neurons are first infected by HSV around the epithelial cells leading to the virus traveling up the neuron and establishing latentcy

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165
Q

Where is latency established by HSV?

A

trigeminal or dorsal root ganglia

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166
Q

What is the bundle of neurons that innervates the face that is infected by HSV? What is the bundle that innervates the genitals?

A

trigeminal ganglia

dorsal root ganglia

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167
Q

When HSV establishes latency, What does the viral genome remain as?

A

an episome

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168
Q

What is the viral genome called when it establishes latency but does not insert itself into the genome?

A

episome

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169
Q

How does a persistant virus overcome elimination by the immune system

A

Immune evasion by counteracting host response
high mutation rates avid host in viruses such as HIV
resides in immuno privileged areas
latent state that limits gene expression to avoid immune system

170
Q

What are the three types of viral infections?

A

acute
chronic
latene

171
Q

What is an acute infection

A

virus replicates rapidly

virus is cleared 1-3 weeks

172
Q

What is a chronic infection?

A

Virus is continuously shedding

infection lasts months to years or even lifetime

173
Q

What is a latent infection

A

No viral shedding
limited gene expression
lasts for the lifetime of host
episodic reactivation

174
Q

What viruses have a chronic infection

A

Hepatitis C/B

HIV

175
Q

What viruses have a latent, reactivation

A

Herpes Simplex virus/ other herpes viruses

VSV (chicken pox)

176
Q
Draw a production over time graph for a:
chronic infection
acute infection
latent/reactivation infection
slow virus
A

refer to flash card

177
Q

What are the problems the acute virus must overcome?

A

Must find next host quickly since the body clears it fairly quickly
must spread easily
must not kill host quickly

178
Q

Describe the polyomaviridae family

A

small, non-enveloped viruses

179
Q

Name some polyomaviridae viruses

A

JC, BK viruses

SV40 the simian virus

180
Q

Why is SV40 often studied?

A

Its role in transformation using the large T antigen

181
Q

What is Merkel Cell carcinoma

A

a rare skin disease that is very deadly

It is thought to be caused by the polyomaviridae Merkel cell polyomavirus

182
Q

What kind of patient is Merkel Cell Carcinoma (MCC) common in?

A

Immunosuppressed patients

183
Q

What are the two liver cell types

A

Hepatocytes (main liver cell)

Sinusoids (thin walled blood vessels of the liver

184
Q

What helps produce extra cellular matrix to provide structural support for the liver

A

Hepatic Stellate Cells, Hepatocytes and liver blood vessels

185
Q

How does an acute liver injury affect the liver

A

the healing response to the wound disrupts the balance between the extracellular proteins and degradation of the proteins by the extracellular protease

186
Q

How does a chronic liver injury affect the liver

A

there is an over expression of the extra cellular matrix that causes fibrosis of the liver

187
Q

What causes cirrhosis of the liver?

A

fibrosis of the liver caused by an over expression of the extracellular matrix proteins

188
Q

What is it called when there is a build up of scar tissue or extracellular matrix that block blood from getting to the liver?

A

Cirrhosis

189
Q

Why is hepatocellular carcinoma a problem

A

Liver cancer is the third leading cause of death in the world

190
Q

What is hepatocellular carcinoma?

A

Cancer of the hepatocytes, which is essentially cancer of the liver

191
Q

What is the most common cause of hepatocellular carcinoma (HCC)

A

cirrhosis of the liver

192
Q

What virus is the major cause of hepatocellular carcinoma?

A

Hepatitis B and C

193
Q

What external factors can increase liver damage by hepatitis B and C

A

Alcohol, it can also cause hepatocellular carcinoma without actually being infected by the liver

194
Q

Do the hepatitis viruses directly cause hepatocellular carcinoma?

A

No even though it contains an oncogene that can directly cause hepatocellular carcinoma (HCC)

195
Q

What does the chronic hepatitis virus do tot he liver?

A

It causes constant cell death of the hepatocytes and the constant regeneration which can lead to mutations in the replication of the genome and ultimatly cancer

196
Q

What increases the risk of cells becoming cancer

A

rapid multiplication caused by replication of cells from viral infections

197
Q

Usually how long does it take for hepatocellular cancer to arise in patients with a chronic hepatitis virus

A

A very long time because you need an accumulation of mutations
Unless you drink alcohol, that makes it go faster

198
Q

Describe the process of a chronic virus causing oncagenesis

A

The constant regeneration of cells due to cell death causes a high risk of mutation due to the need for rapid replication. This over time will lead to an accumulation of mutations that will eventually promote one cell to become oncogenic and thus causing cancer

199
Q

What family is the hepatitis virus B in?

A

Hepadnaviridae

200
Q

What is the structure of the hepatitis B virus?

A

Enveloped virus

201
Q

What is unique about the hepatitis B virus?

A

It goes through an RNA stage making a DNA retrovirus

202
Q

What virus is the most common cause of chronic liver infection?

A

Hepatitis B

203
Q

What genes does the hepatitis B virus encode?

A
Pol (RNA and DNA dependent DNA)
Core (capsid protein)
S protein (surface antigen (envelope)
HBV X (signal transduction and transcription factor)
HBV e (secreted form of C protein)
204
Q

Describe the process of Hepatitis B replication

A

Double stranded DNA enters the nucleus and then circularizes where ithe (-) DNA will make mRNA to create the coat protein. Then the RNA is reverse transcribed by the reverse transcriptase from the virus and then that DNA is packaged (The partiall double stranded DNA

205
Q

What is the major rout of transmission of the Hepatitis B virus (HBV)

A

Sexual transmission
maternal to fetal
breast milk, blood, tear fluid

206
Q

What bodily fluids can contain infectious hepatitis B virus?

A

Serum, urine, saliva, nasal secretions, vaginal secretions, and seman

207
Q

What is more infectious if you accidentally used a contaminated needle, HIV or HBV

A

Hepatitus B virus, you have about a 40 percent chance of getting it, while for the HIV virus you have about a 0.3 %

208
Q

What induce hepatitis when infected by the hepatitis B virus?

A

The immune system causes the damage on the liver

209
Q

Does the Hepatitis B virus directly cause hepatitis to arise?

A

No it caused by the immune system, the Hepatitis B virus does not actually lyse the cell, it is an enveloped virus that just buds from the cell

210
Q

Where does the Hepatitis B virus replicate?

A

In the hepatocytes in the liver

211
Q

What HBV antigens appear in the serum during the disease?

A
HBV S protein (surface)
HBVe antigen (soluble form of core protein that can be found in the blood
212
Q

What happens to ALT and AST levels when the HBV DNA disappears

A

It increases and the patient will get jaundice

213
Q

What is a major complication of the Hepatitis B virus infectioon?

A

Fulminant hepatitis (1%) and chronic hepatitis(5-10%) but this usually both happens in a small number of partients diagnosed in the virus

214
Q

What is Fulminant Hpeatitis?

A

Acute liver failure which eventually leads to death and in rare cases is caused by the hepatitis B virus

215
Q

How does a chronic infection of Hepatitis B virus arise, that generally leads to hepatocellular carcinoma?

A

If there is a lack of immune control that will generally lead to a chronic infection
-if the patient is immunosuppressed or a male

216
Q

What is the major complication with Chronic Hepaititis B virus?

A

Cirrhosis and hepatocellular carcinoma

-This is usually accelerated with alcohol

217
Q

What is one way to treat hepatocellular carcinoma?

A

liver transplant

218
Q

What are the two direction toward disease that chronic hepatitis can become

A

Persistent hepatitis which can eventually lead to aggressive hepatitis, leading to cirrhosis

219
Q

Describe the Diagnosis of the hepatitis B virus

A

You can use serology to analyze HBV S and C (the surface and the coat protein), you can also look for HBV A and HBV A in the blood at high levels (antibodies)
-You can also use genome amplification by doing PCR of the viral DNA in the blood or you can look at the amount of virus you have in the liver by doing a liver biopsy

220
Q

Does the hepatitis B virus have a vaccine?

A

Yes

221
Q

What does the Hepatitis B vaccine consist of?

A

recombinant hepatitis B surface antigen

222
Q

How is the Hepatitis S antigen made for the hepatitis B vaccine?

A

purified yeast

223
Q

How is the HBV vaccine administered?

A

there are three doses that is give at 0, 1, and 6 months

224
Q

Why is a cure for the HBV virus hard to come create?

A

because the DNA of the Hepatitis B virus is circularized

225
Q

What does the treatment for chronic hepatitis B virus consist of?

A

These are drugs used to decrease chronic replication of the virus but it is not a cure so it must be taken for a long period of time

  • You can also use interferon Alpha treatment but it is not virus specific
  • lamivudine (3TC) which is a a nucleoside analog Reverse transcription inhibitor
226
Q

What is Hepaititis Delta

A

it is not a virus but a sub-viral particle because it does not have a viral attachment protein or a polymerase

227
Q

Which hepatitis virus is not an actual virus

A

Hepatitis Delta since it does not have a virus attachment protein or a polymerase

228
Q

What does HDV require to infect a cell

A

Infection by HBV since it borrow the envelope proteins of the HBV virus to move from cell to cell

229
Q

What are the two patterns for hepatitis D virus infection?

A

Co-infection and super infection

230
Q

Describe the co-infection of the hepatitis D virus

A

When both HBV and HDV infect at the same time

231
Q

Describe the super infection pattern of the Hepatitis D virus

A

This is when HDV infects a previously chronically infected HBV patient

232
Q

Why is a super infection pattern of HDV dangerous

A

It increases chances of getting a fulminant disease and it creates the presence of HBsAg causing an immediate spread of HDV in the body

233
Q

Discuss the diagnosis of the hepatitis D viris

A

You can use serologic assay to look for Delta antibody -IgG and IgM and RNA from the virus

234
Q

What is the treatment for the hepatitis D virus?

A

There is no treatment

235
Q

Why is it hard to create a treatment for the hepatitis D virus?

A

Because the hepatitis B treatment does not target the Hepatitis S protein or production and HBV S is needed for HDV infection

236
Q

What is the prevention method for hepatitis D

A

Use the hepatitis B vaccine

237
Q

How was the Hepatitis C virus identified?

A

Through molecular biology methods and this was the first virus found this way

238
Q

What family is the hepatitis C virus in?

A

flaviviridae

239
Q

What is the Hepatitis C virus genus

A

Hepacivirus

240
Q

How is HCV transmitted?

A

it is a blood borne virus

241
Q

What is the leading cause of HCV?

A

injection drug abuse

242
Q

What are the rare ways that hepatitis C may also be transmitted?

A

Hospital needles
tatoos
vertical transmission
Sexual transmission

243
Q

What are the two types of HCV disease and which one is most common?

A

Acute and chronic infection and the chronic infection is more common

244
Q

Describe the acute infection of the hepatitis C virus

A

HCV will replicate in the hepatocytes with symptoms usually being. mild or absent Jaundice may occur

245
Q

Describe the chronic infection of hepatitis C

A

HCV will constantly replicate in the hepatocytes allowing for persistent viremia
-a mild disease willusually occur that will lead to inflammation of the liver and a mild increase in ALT

246
Q

What increases the damage done by the hepatitis C virus

A

Alcohol and having a suppressed immune system

247
Q

Discuss the epidemiology of the Hepatitis C virus

A

this is seen world wide

248
Q

What is the most common cause for a liver transplant in the US

A

Hepatitis C

249
Q

How many major genotypes of HCV is there

A

6

250
Q

How is HCV diagnosed?

A

you look for HCV antibodies
you can also check for viral RNA in the blood through the use of PCR
-Here you cannot really look at ALT to determine how severe the case is

251
Q

Discuss the treatment of HCV

A

You can use interferon therapy to treat the chronic infection
-you can also give a combination of both Pegylated IFN and Ribavirin

252
Q

What is the problem with HCV drug therapy?

A

Nearly half of all the patients do not respond to the therapy and are therefore not cures
-also interferon and ribavirin have awful side effects such as malaise and flu like symptoms

253
Q

What is the new drug used to cure HCV?

A

It is called Harvoni, which is a combo drug, that works as an inhibitor, and it uses NS5A inhibition

254
Q

Discuss the difference in rates of chronic infection between hepatitis B and hepatitis C

A

Hepatitis C has an overwhelmingly large amount

255
Q

What is unique about the hepatitis C virus

A

it is a blood borne hepatitis virus

256
Q

What is unique about the retroviridae that is not seen in other viruses?

A

It is a diploid virus meaning it has two copies of its (+)ssRNA

257
Q

Why is the retroviridae called retro?

A

Because the RNA must use a reverse transcriptase in order to make DNA from the RNA and then make the protein

258
Q

Why do the retroviride go through the process of revers transcription?

A

So that it can incorporates its DNA into the DNA of the cell

259
Q

What are the two types of Retroviridae?

A

Simple retrovirus and complex retrovirus

260
Q

What viruses are under the category of simple retroviruses?

A

Alpharetrovirus
betaretrovirus
gammaretrovirus

261
Q

What is unique about the genome of simple retroviruses?

A

It has long terminal repeats on each side that is needed for replication

262
Q

What are the three genes made by the simple retrovirus genome?

A

gag: group associated antigens
pol: polymerase
env: Envelope

263
Q

How does the retrovirus enter the cell?

A

Through fusion

264
Q

What gene is involved in retrovirus entry?

A

Env which creates 2 subunits, which are the viral attachment protein and the fusion protein (

265
Q

What is the retrovirus lipid envelop contain?

A

trimer which are 3 copies of hetero-dimers. The heterodimers areboth the SU and TM protein combined

266
Q

Where does fusion occur for the retrovirus?

A

At the plasma membrane of in the endocytic vesicles

267
Q

Describe the process of Retrovirus fusion

A

The SU protein will bind to the cell membrane where a hair pin will form by the trans membrane protein in order to allow fusion

268
Q

What protein of the retrovirus allows for fusion?

A

The transmembrane protein

269
Q

What is peculiar about the fusion mechanism of viruses?

A

It is conserved among other viruses

270
Q

What Retrovirade protein allows for integration of the viral genome into the cell genome?

A

Integrase

271
Q

What important virus particle must be packaged inside the retrovirade?

A

A reverse trannscriptase and integrase

272
Q

In terms of infection what is the difference between the simple retrovirus and the complex retrovirus?

A

The simple retrovirus requires cell division

-The complex retrovirus can successfully infect on-dividing cells

273
Q

When the genome is integrated into the host cell, what is this called?

A

provirus

274
Q

What happens to a cell with a provirus during division?

A

During division that means the virus will replicate as well

275
Q

Is the retrovirus site specific?

A

There are usually no specific target sites by the virus

276
Q

What happens after retrovirus integration in the cell?

A

Transcription

277
Q

How are the protein transcribed in the retrovirus

A

ASK

278
Q

Describe the maturation process of the retrovirus

A

Gag is cleaved by the viral protease into separate protein after budding

279
Q

What proteins are cleaved during the maturation of the retrovirus?

A

Matrix (ma)-lies underneath the lipid envelope
Capsid (CA) whcih forms the shell of the protein
Nucleocapsid (NC)

280
Q

What makes a retrovirus not infectious?

A

When it has yet to undergo maturation

281
Q

What did retrovirologists discover that became revolutionary to how we study genes?

A

The oncogene because the avion retrovirus carried an oncogene to induce carcinoma

282
Q

What is the normal version of an oncogene called?

A

A proto-oncogene

283
Q

what is it called when a cell becomes cancerous?

A

transformation

284
Q

Describe the acute transforming retroviruses

A

This is when the retrovirus that infects a cell directly carries a proto-oncogene with it, most are defective

285
Q

What makes a retrovirus defective?

A

Usually the gag or pol or env gene is replaced with an oncogene and it therefore requires another retrovirus infection to allow for the over-expression of the oncogene

286
Q

How long is the time for tumor formation when infected with an acute transforming retrovirus?

A

usually weeks

287
Q

Describe how the Non-transforming retrovirus causes cancer?

A

This induces cancer through indirect induction. The retrovirus is integrated near a proto oncogene causing the induction of an oncogene

288
Q

Why is retroviral therapy a problem?

A

Because there is a chance of indirect induction of tumors where the retrovirus will integrate its genome at a proto oncogene

289
Q

What makes up a huge portion of the human genome?

A

Human endogenous retroviruses

290
Q

Can human endogenous virus be reactivated?

A

Very few can

291
Q

What RNA viruses can causes cancer?

A

Retroviruses

292
Q

What is HTLV

A

Human T lymphocyte virus

293
Q

What kind of virus is the human T cell Leukemia virus?

A

A deltaretrovirus

294
Q

What genes doe the Human T leukemia virus contain (HTLV)

A
Gag
pol
env
tax
Rex
295
Q

What does the Tax protein in Humant T leukemia virus do?

A

It is a transcriptional activator of viral RNA and it works like an oncogene in cell culture by activating cellular genes and signal transduction

296
Q

Discuss the Epidemiology of the Human T leukemia virus

A

it is endemic in sub-saharan africa, japan and the pacific, the caribean, south and central america

297
Q

What is the Human T leukemia virus related to?

A

Simian T cell leukemia virus giving us the idea that it probably rose from a zoonotic event

298
Q

What is a big complication with human T leukemia Virus?

A

Aggresive adult T cell leukemia

299
Q

What are the characteristic of aggressive adult T-cell leukemia?

A

It will produce skin lesions which is why it is also call cutaneous T cell lymphoma. I also cause mild immunodeficiency without cancer
It can also cause chronic myelopathy or tropical spastic paraparesis which is an inflammatory disease

300
Q

What cell does the human T leukemia virus infect

A

CD4+ T cells

301
Q

Describe the diagnosis of the HTLV virus

A

You can use elisa for antibodies

-PCR of provirus of viral genome

302
Q

Discuss the transmission of HTLV

A

This virus is highly cell associated so there is little virus found in fluids
primarily mother to child through breastfeeding
sexually
infected blood to blood products
sharing needles

303
Q

What is the treatment for the HTLV

A

There is no vaccine but you can treat the cancer

304
Q

Where can you get HTLV 2

A

From a T cell hairy Leukemia

305
Q

What is HTLV-3 called now?

A

HIV-1

306
Q

What is gene therapy

A

This is when you insert a functioning gene into cel with a certain dysfunction so that you can increase its cellular function

307
Q

What is the gene inserted in gene therapy called?

A

A transgene

308
Q

Why would you want to add a gene to a cell?

A

The absence of that gene in the cell causes disease and you want to fix it

  • you can make the cell more sensitive to a drug to target disease
  • you can make the immune system target the specific cell
  • or you can induce cell proliferation for tissue repair
  • you can even delete a gene
  • increase p53 function
309
Q

How do you add a gene to a cell?

A
Ex vivo (out of the body where you remove a cell from the body and put the gene into it, then insert the cell into the patient)
In vivo (in the body where you inject a vector into the patient that will essentially put the gene into the person bu there are issues with targeting efficiency and the immune response)
310
Q

What is a vector in terms of gene therapy?

A

In gene therapy this is an agent that transfers genetic material from one cell to another

311
Q

What are the three types of vectors

A

Viral vector
Non-viral vector
combination vector

312
Q

What is a viral vecto

A

A virus where the genome has been altered so that it codes for extra genes

313
Q

What are the limitations to using a viral vector

A

It has tropism and immune recognition

314
Q

What is a non-viral vector

A

This is not as efficient as using a virus vector, it has less immune recognition, it is expensive and it can be naked DNA

315
Q

What is a combination vector?

A

This is trying to mix both the viral and non-viral vector but it is still under development

316
Q

What are the two types of viral vectors?

A

Defective and replication competant vectors

317
Q

What kind of viral vector is modified so that it cannot replicate on its own?

A

A defective vector

318
Q

Describe a defective vector

A

Where the insertion of the new viral vector does not result in replication of its own.
This works like an acute transforming retrovirus

319
Q

What are replication competent viral vectors?

A

Vector that are inserted in the genome, but it has the capabilities replicating on its own because there is enough in the viral genome to support replication

320
Q

Why is a defective viral vector safer?

A

There is a fear that the replication competent viral vector will have the capability of producing viruses that will be able to revert and create a virus that will cause disease in the person

321
Q

What viruses are used as a viral vector?

A
adenovirus
retrovirus
adeno-associated virus
poxvirus
herpesvirus
322
Q

Why was there a failure in gene therapy in 1999

A

the immune response was so strong that it lead to organ failure

323
Q

What caused the first success in gene therapy?

A

using a retrovirus ex vivo where the cells where then put back into the patient

324
Q

What category of retrovirus is HIV in

A

complex retrovirus

325
Q

In HIV what proteins are made by the gag complex?

A

MA-matrix
CA-capsid (p24)
NC-nucleocapsid

326
Q

What does the HIV matrix protein do?

A

coats the inside of the envelope and helps the DNA get into the nucleus

327
Q

What does the HIV capsid protein do?

A

It forms a shell around the genome

328
Q

What does the HIV nucleocapsid protein do?

A

binds to genomic RNA

329
Q

What proteins in HIV are part of the pol group of genes?

A

PR-protease
RT-reverse transcriptase
IN-integrase
-functions of these proteins are self explanitary

330
Q

What proteins are part of the env complex of proteins

A

SU-surface protein (gp120)

TM-trans-membrane protein

331
Q

What does the HIV SU protein do?

A

it binds to the receptors on the cell

332
Q

What does the HIV TM protein do

A

trans-membrane protein and it mediates fusion of the virus

333
Q

What does the vpr HIV protein do?

A

virion protein R and it facilitate nuclear entry of DNA before integration

334
Q

What is HIV gp120

A

the surface protein

-stands for glycoprotein

335
Q

what is HIV gp41

A

the protein that mediates fusion

-stands for glycoprotein

336
Q

what are the function of the nonstructural protein in HIV

A
  • There is a protein that inactivates host defenses
  • there is a protein that promotes receptor degredation and inactivate the host defenses
  • a protein that up regulates the transcription of HIV genes
  • a protein that plays a role exportin the spliced and unspliced mRNA
  • there is a protein that regulates MHC 1 and CD4
337
Q

When the HIV viral genome is first transcribes what does it make

A

two mRNAs, on for gag-pol and one for Env

338
Q

What is unique about the HIV virion?

A

it has a strange nucleocapsid shape, almost like a chip

339
Q

Describe the pathogenesis of the HIV infection

A

first the virus will enter the mucosal surface but it does not infect the epithelial cells instead it will attach to the dendritic cells, but again it does not infect it. Then the dendritic cell will bring the virus to a CD4+ T cell in the lymph node where the virus will then replicate in the blood. The lymphatic tissue will then move thorugh out the bod and infect the lymphatic tissue. The biggest cell it infect are the GALT cells

340
Q

Why does HIV mainly infect the GALT cells?

A

These are the gut associated lymphoid tissue and this is because there is a large abundance of CD4+ T cells

341
Q

After HIV is cleared from the body by the immune system, where does the virus still replicate?

A

lymph nodes and GALT

342
Q

What does the constant HIV replication in lymph nodes and GALT lead to?

A

The CD4+ T cells over time will degrade leading to a large spike in viruses and a huge increase in viral replication

343
Q

What is the major cause of infection by HIV patients?

A

A depletion of the immune response due to the death of CD4+ T cells in lymph nodes and GALT cells

344
Q

What are the two types of HIV-1

A

R5 tropic (M tropic) and X4 virus (T tropic) and this is based off of the co-receptor or the trans-membrane protein on the virion

345
Q

What are the differences between X4 HIV virus and R5 Tropic HIV virus

A

The M tropic one is the transmitted virus and it can infect macrophages

346
Q

Be able to draw the immune response to HIV graph

A

look at graph

347
Q

Name the phases of the HIV infection

A

flu-like disease
asymptomatic phase
symptomatic phase
aids

348
Q

What happens in the flu-like phase of HIV or primary infection

A

fever, swollen lymph nodes, flu-like symptoms

349
Q

What happens in the asymptomatic phase of an HIV infection?

A

no disease

350
Q

What happend in the symptomatic phase/AID of the HIV infection

A

immunosuppression that will ultimately lead to death in the patient

351
Q

What usually determines how long it will take for HIV to become full blown AIDS?

A

how long it takes to clear the primary infection. This is known as the set point, and the shorter it is, that is how good your immune system

352
Q

What is the set point in an HIV infection?

A

This is how high the viral lead is at the end of the asymptomatic phase. The higher, the faster the progression to AIDS

353
Q

During an HIV infection discuss how the CTL corresponds to the progression of HIV to AIDS?

A
strong CTL (CD8+ T cell) response will cause a slower progression because it means you have a strong immune system
-a weak CTL response with a strong antibody response means that you do not have enough cytotoxic T cells in your body causing a fast progression to AIDS
354
Q

what kind of people have a faster progression to AIDS from HIV?

A

infants, transfusion recipients, hemophiliacs

355
Q

What are the patterns of progression in HIV infections?

A

Fast progressors
slow progressors
long term non progressors
elite controllers

356
Q

What does it mean to be a long term non progressor with an HIV infection

A

This means that you have a detectable virus but you do not have a decrease in the CD4+T cell count

357
Q

What is an elite controller in an HIV infection?

A

A person who is infected but there is no virus in the plasma so the infection never proceeds to AIDS

358
Q

What happens during the AIDS infection

A

the immune system is destroyed by AIDS because of the death of CD4+ T cells which will affect the CD8+ cells and B cells. This cause what would normally be a small disease in people an opotunistic infection

359
Q

What is an opotunisitic infection

A

In AIDS patients, when the disease has been compromised so much,even a small infection will cause a large infection and cause the disease to go wild

360
Q

What are the variations in HIV called?

A

Clades

361
Q

What are the three major genetic lineages of HIV?

A

M (major)
O (outlier)
N (non-M, non-O)
the different variants in these are called sub types or clades

362
Q

What virus is HIV related to?

A

Simian immunodeficiency virus in non-human primates showing that this probably came from zoonotic transmission

363
Q

What is different in SIV in their hosts as compared to the HIV infection in humans?

A

the SIV virus is asymptomatic in their hosts, but when chimpanzees acquire this virus it is not symptomatic

364
Q

What happens when a chimpanzee gets SIV from monkeys?

A

It will not be asymptomatic and the Chimpanzee will get AIDS

365
Q

How is HIV spread in adults?

A

Sexual contact through genital secretions
injection drug use and unsteralized needles
contaminated blood through hospital procedures
-transplant of organs
-these transmission routes change throughout the world

366
Q

How can you reduce transmission of HIV

A

Use condoms and male circumcision may decrease the risk, due to lower CD4+ cells

367
Q

How is HIV transmitted to children?

A

in utero
through blood
genital secretions
breast milk

368
Q

How can a mother decrease the risk of transferring HIV to her child when pregnant?

A

antiretroviral therapy

369
Q

What is the problem with the vertical transmission of HIV?

A

the time it takes to become full blown aids is highly shortened

370
Q

Discuss HIV diagnosis

A

Detection of anti-HIV antibodies by looking at blood using ELISA test
There is also a home rapid response test

371
Q

What is hard about HIV diagnosis?

A

It takes about four to six weeks to get antibodies and sometimes it can take up to 6 months

372
Q

When the HIV virus is diagnosed, what guide therapy is followed

A

quantitative PCR for viral load
CD4+T cell count
assay for drug resistance of virus

373
Q

Where is HIV in greatest amount?

A

Sub-saharan africa

most prevalent in low and middle income famalies

374
Q

What characteristic about HIV that makes finding an effective vaccine or treatment difficult?

A

The fact that it replicates and evolves at an enormous rate

375
Q

due to the high mutation rate of HIV, what kind of species are created?

A

Quasi-species

376
Q

Why do people nee long term drug treatment of HIV?

A

the infected cells harbor the latent virus and activation can occur slowly over the years

377
Q

What is one of the most effective treatments for HIV

A

highly active antiretroviral therapy

HAART

378
Q

What is HAART

A

Highly active antiretroviral therapy where it contains multiple types of HIV drugs. It includes two reverse transcriptases and an integrase inhibitor and a protease inhibitor

379
Q

What is the problem with long term antiretrovial drug usage?

A

difficult to maintain constant pill habit

  • cost
  • a lot of side effects
380
Q

What is Pre-exposure Prophylaxis?

A

This is when you use HAART before HIV exposure to reduce the risk from getting HIV at high risk
The drug is called truvida

381
Q

What has gone wrong with giving babies HAART soon after birth in high risk mothers

A

there are many reports of the virus rebounding in the kids

382
Q

What was the proposed vaccine for HIV?

A

Sanofi/Vaxgen

383
Q

Describe the assumptions with Sanofi/vaxgen

A

It tried to insert some of the HIV genes into the canarypox virus

384
Q

What was the outcome for the Sanofi/Vaxgen vaccine experiment

A

It was statistically significant in preventing HIV but it was not that impressive data
-It had no effect on CD4+ T cell count

385
Q

Describe the HIV-2 virus in broad terms

A

found in west africa
much less common than HIV-1
-thought to arise from a different primate species
-usually more controllable

386
Q

What is a strong indicator for HIV prognosis

A

Set point

387
Q

What is the largest human Virus?

A

poxviridae

388
Q

Describe the viral structure of the poxviridae

A

It is neither icosahedral nor is it helical, it is a shape of its own

389
Q

What DNA virus replicates in the cytoplasm of the cell?

A

poxviridae therefore it must have its own RNA polymerase

390
Q

What are the unique features of the poxviridae?

A

It replicates in the cytoplasm even though it is a DNA virus

  • The ends of the DNA strand are connected to the complementary DNA, they are fused
  • It has a different subset of capsid shape, looks like a brick
  • It is the largest human virus
391
Q

What poxviruses are obligate human pathogens?

A

Variola virus

mollusca contagiosum virus

392
Q

What family is mollusca contagiosum in?

A

poxviridae

393
Q

Describe the disease of mollusca contagiosum

A

It is very mild pox virus that causes a very mild skin disease with raised pink bumps on the skin

394
Q

How is mollusca contagiosum spread?

A

From skin to skin contact (Wrestlers get this quite often)

-By scratching or picking the bump

395
Q

How are immunosuppressed patients affected by molluscum contagiosum?

A

they usually just get larger growths

396
Q

Where doe Molluscum Contagiosum occur?

A

All over the world

397
Q

How is molluscum Contagiosum diagnosed?

A

Usually isn’t because it is so mild

398
Q

What is the treatment for molluscum contagiosum?

A

Similar for the human papilloma virus, cryotherapy or sialicylic acid treatment, but it usually isn’t treated because it is so minor

399
Q

How is the variola virus and molluscum contagiosum different in terms of scarring?

A

Molluscum contagiosum virus does not leave scars while the variolla virus does

400
Q

What family and genus is the variola virus in?

A

Family: poxviridae
genus: Orthopoxvirus

401
Q

What are the two major types of variola virus?

A

variola major (30% fatality) and variola minor (1-2% fatality)

402
Q

Which variola virus major type is most fatal?

A

variola major

403
Q

How was the variolla virus spread?

A

through inhalation of the virus in the respiratory tract

-it is very weakly spread as a fomite

404
Q

What disease does the variolla virus cause?

A

Small pox

405
Q

Describe the pathogenesis of the variolla virus

A

First the virus is inhaled and begins to replicate in the upper respiratory tract. The virus is the disseminated through viremia. The is then infected during secondary viremia. The pox will then rise all over the body, often leaving scars if the patient survives

406
Q

Where is the variolla virus now?

A

small pox disease has been eradicated from the world, although two samples are stored in CDC and in Russia

407
Q

Where does the vaccine for the variola virus come from?

A

the Vaccinia virus because the two viruses are homologous and they share a few of the same antigenic determinants

408
Q

What is common in both the vaccinia virus and the variola virus?

A

antigenic determinants

409
Q

What is are the proteins that antibodies are made to called?

A

antigenic determinants

410
Q

What was the original method of vaccination called?

A

Variolation

411
Q

How did the vaccinia virus come about?

A

when Jenner found out that you can treat cowpox by taking some of the lesions and giving it to people in order to illicit an immune response. They got the name from the word for cow

412
Q

what was used to prevent the variola virus?

A

Vaccinia virus

413
Q

What are the dangers with the vaccinia virus

A

one in a million people dies from complications with the vaccine

  • The major side effects include large sores and heart problems
  • people with eczema should not be given the virus because this can cause a life threatening pox all over the body
414
Q

What is necessary for eradication of a virus?

A
No animal resivoir
minimal serotypes that cause disease
-no persistance
-causes acute recognizable spread
-You need the world to eliminate it which costs a lot of money
415
Q

What made it possible for the eradication of smallpox?

A
  • The vaccine worked for variola virus and it only has one major serotype making the vaccine simple
  • the disease is also easily diagnosed based on the scars, and there is no long term persistance with the disease
  • There is no animal host reservoir
  • The disease was so bad that all of the world was willing to promote elimination
416
Q

How is the monkey pox virus spread

A

from prairie dogs to humans (came from zoonotic origins

417
Q

Describe the disease of monkey pox

A

it is a more mild form of small pox

  • fever, headache, swollen lymph nodes
  • rash
  • the pox will crust over leading it to be cleared in about 2 to 4 weeks
  • can be lethal
418
Q

Where is monkey pox endemic?

A

Africa (fatality rates usually center around here

419
Q

Why was there a rise in monkey pox?

A

we no longer use the vaccinations for small pox therefore there is no protection against monkey pox

420
Q

Why is the variolla virus a fear in bioterror?

A

It is very easily disseminated to people. It causes high mortality rates and outbreak would cause major panic

421
Q

What are the three classes for potential viral bioterror agents?

A

Class A: agents that provide the similar aspects of disease as the variola virus
Class B: Viral encephalitis (moderately easy to spread with moderate death rates)
Class C: Emerging viruses