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D/T 1 > Exam 2 week 2 > Flashcards

Exam 2 week 2 Flashcards

1
Q

Which viruses depend on host DNA dependent DNA pol

A

Parvo papilloma polyoma

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2
Q

define eclipse period

A

time from infection to detection of new virus

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3
Q

define latent period

A

time from infection to detection of EXTRACELLULAR virus

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4
Q

burst size

A

amount of new virus from a single infected cell

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5
Q

what are the receptors for HIV virus

A

Primary- CD4, secondary= CCR5, CXCR4

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6
Q

EBV receptors are

A

primary CD21, secondary MHCII

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7
Q

Influenza receptors are

A

terminal salic acid on glycolipids or glycoproteins

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8
Q

rhinovirus receptors

A

ICAM1

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9
Q

rabies virus receptors

A

nACHr, NCAM

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10
Q

measles receptors

A

CD46, CD150

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11
Q

what is tropism

A

the kind of cells a virus can infect depending on the host cell receptor expression

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12
Q

How do enveloped viruses enter cells

A

1) viral lipid membrane merges with PM of host cell and releases nucleocapsid into the cytoplasm.
2) endocytosis of virus, low pH of endosome allows fusion to the endosomal membrane and release of nucleocapsid to the cytoplasm

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13
Q

how do naked viruses enter cells

A

by endocytosis. the low pH of endosome changes the capsid and release of material to cytoplasm

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14
Q

what is uncoating

A

the release of genetic material from the nucleocapsid. Reo is loose capsid

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15
Q

how does herpes reproduce

A

enters cells and uses RNA poll to make TF and DNA pol

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16
Q

how does polyoma and papilloma replicate

A

they do not have or encode viral DNA pol. they need to activate the cell in order to get viral DNA replicated

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17
Q

Which viruses uses their own pol to copy genetic material. why is it important

A

Adeno, herpes, pox, hepadna have own DNA pol. The DNA pol is a great target of antiviral therapy

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18
Q

What viruses do not have own virally encoded pol? How do they replicate

A

Papillomo, polyoma and parvo. Papilloma and polymer kicks the cells into S phase to replicate. Parvo must enter actively dividing cells.

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19
Q

What is the replication for Pox viruses like

A

Exception: DNA virus that carries their own RNA Pol in the virion can replicate in the cytoplasm. Have a complex envelope

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20
Q

What is notable about HBV/hepadna

A

HBV is replicated in both the nucleus and the cytoplasm. It replicates DNA genome through RNA intermediate via own reverse transcriptase. NTRIs can be used in therapy

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21
Q

What is notable about herpes virsus

A

it can enter latent period for years like shingles and cold sores

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22
Q

How do +ssRNA replicate

A

They can be made directly into mRNA. They make polyproteins that need to be cleaved by viral proteases (all +ssRNA viruses have viral proteases) and viral RNA dependent RNA pol is made. The viral RNA pol can make both mRNA and -ssRNA.
GOOD TARGET FOR THERAPY IS PROTEASE OR POLYMERASE

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23
Q

What type of pol do +ssRNA viruses use

A

they encode (don’t bring in) their own RNA dependent RNA pol.

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24
Q

How do retroviruses replicate

A

Retroviruses- HIV and HTLV convert +ssRNA into 2 copies to make DNA (called diploid). Proviral DNA integrates into the host cell DNA via integrate and remains for the life of the cell.

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25
Q

How do -ssRNA replicate

A

viral RNA pol must first make mRNA from -ssRNA. VIRAL RNA pol MUST BE INCLUDED IN THE VIRON.

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26
Q

what is special about orthomyxoviruses

A

they are -ssRNA viruses with replication in both the nucleus and the cytoplasm.

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27
Q

what is special about HDV

A

it is a -ssRNA virus that has no viral pol. must use cell machinery. Also no enveloped glycoprotein so can’t make infectious visions without co-infection with HBV to use HBsAg as viral envelope glycoproteins. HDV cannot replicate on its own.

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28
Q

what is special about Reovirus

A

is naked, segmented genome, and contains viral RNA pol in its iron. It MAKES dsRNA!!!

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29
Q

Assembly- what DNA virus not in nucleus. which self assembles

A

Pox not in nucleus

papilloma capsid self assembles

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30
Q

How do naked viruses bud

A

they escape when the cell dies or through vesicular transport

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31
Q

How do enveloped viruses bud

A

They assemble their virion as they acquire the cell lipid membrane that has viral envelope glycoprotein. the cell lipid bilayer is usually from the plasma membrane.

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32
Q

How do DNA viruses obtain mutations to change and escape antiviral= genetic shift

A

through strand breakage or homologous/non homo recombination. results usually defective

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33
Q

How do RNA viruses obtain mutations= genetic shift

A

through strand jumping of RNA pol and recombinations homo and non homo. results usually defective

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34
Q

what viruses use gene resortment as a genetic shift

A

must have segmented genome and two strains infect same cell. Influenza makes viruses with different neruaindase and hemaglutin. difficult to make vaccines and can lead to pandemic. also Reovirus

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35
Q

what has the highest mutation rate

A

RNA viruses d/t the RNA pol lacking proofreading ability. Then the more complex the more stable

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36
Q

What is a quasi viral species and why is it important to therapy

A

The host viruses are not identical to but slightly different. When antiviral therapy is started there may be a mutant resistant to the therapy present making combination therapy important

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37
Q

What are some defective viruses

A

HDV and aden associated viruses. on their own they are not infectious. need co-infections to spread.

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38
Q

what is a defecitve interfering particle

A

they interfere with the growth of the virus and can’t replicate on their own without complement virus. they take up resources needed by WT virus

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39
Q

polypoidy

A

more than one copy of genome is packaged from the same virus

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40
Q

heteroploidy

A

two viruses infect the same cell and the virus packages more than one genome, one from each virus

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41
Q

phenotypic mixing

A

two viruses infect the same cell and the resulting A virus has the viral proteins from virus B or a mixture of viral proteins from virus A and B but the genome from virus A.

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42
Q

pseudotyping

A

two viruses infect the same cell, virus 1 acquiers glycoprotein from virus 2. this new virus can infect cells with the receptor tropism for virus 2. however if new viruses are produced they will have virus 1’s glycoprotein and 1’s tropism

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43
Q

Define lytic

A

virus lyses from cell killing it in the process

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44
Q

define cytopathic/cytocidal

A

kills cell but not necessararily from lysis. could be a by product released

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45
Q

Latent virus is an important part of what virus

A

are not productive- do not produce virus and non cytocidal. herpes virus is latent. stimuli can activate into reproductive cycle

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46
Q

Syntcia formatioin

A

when infected cell membrane of neighborning cells fuse to form a MULTINUCLEATE cell

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47
Q

Describe virally transformed cells

A

Virally transformed cells have no contact inhibition. the cells grow on top of each other. they can grew indefinetley and cause tumors when injected into animals. The cells have altered cell morphology

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48
Q

What uses are there for growing viruses in cell culture

A

It is useful for diagnostic tests and needed for some vaccine production

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49
Q

what important cells are used in cell culture for viruses

A

Primary cells, Human diploid cells- kidney and fibroblast cells from embryonic tissue, are safer than the immortal cell lines of humans and can grow for 20-50 divisions, used for vaccines.
Immortal cell lines- can grow indefinetly, useful for growing virus and diagnostic virology

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50
Q

What vaccines used human diploid cells

A

adenovirus, HAV, polio, rabies, rubella, varicella (chicken pox and shingles)

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51
Q

What vaccines use chicken embryo fibroblast

A

measles and mumps

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52
Q

what vaccines use embryonate chick eggs

A

influenza and yellow fever

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53
Q

Why is diagnostic virology useful

A

used to confirm and dx, rx for antiviral drugs, monitor chronic infections and epidemlogical monitoring

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54
Q

What is EM used for

A

EM can be used for fecal samples but nucleic acid detection techniques are often used now

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55
Q

Cytology- what is it and what diseases is it used in?

A

Look for presence of viruses in patient sample but usually not very specific. Inclusion bodies in HSV encepholitis and CMV owl eyes. Tzanck smears in herpes simplex virus and VZV from lesions

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56
Q

What is DFA and what is it used for

A

Direct fluorescence antibody test- DFA binds antiviral antibody to tissue of cell without culture. If positive test more for type of virus. if negative deterimine if true negative by cell culture or nucleic acid amplification test.

It depends on the antibody detecting the virus. if there is divergence in the virus like in influenza then antibody might not recognize the virus. not corona or rhino but influenza and rabies and other

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57
Q

What are drawbacks to cell culture test

A

the cells must be permissive to infection, still need to confirm with other tests, takes weeks and expensive

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58
Q

What is a hem absorption test

A

Viral hemaglutinin expressed on the surface of the infected cells can bind RBC. If a cell infected with one of the viruses that expresses hemaglutinin these cells will bind RBC. Most useful for influenza, parainfluenza, mumps

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59
Q

What is a rapid culture shell via spin amplificiation

A

a viral sample is added to a tube that has a cover slip. the culture is 16hr to 5 days. presence of virus by fluorescent abs

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60
Q

What are neutralizing abs and what tests use them

A

neutralizing abs bind to outside of virus and prevent infection of cell. enveloped=glycoproteins, naked=capsid proteins

Can type virus by blocking plaque formation-CPE, synctia, or immunoflorense. or block hem adsorption which is useful in deterring viral type in hemaglutination assay and quick way for influenza type

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61
Q

hemagglutination assay

A

RBC will clump together normally. Add viruses that bind RBC and will prevent clumping and diffuse the cells. eeasy 30 min test for influenza

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62
Q

Hemagglutination inhibition assay

A

If the virus is incubated with the correct neutralizing ab it will not bind to the RBC and the cell will look negative for virus- useful in influenza or titer neutralizing ab

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63
Q

What does ELISA or EIA detect

A

detects IgM for acute infections and IgG for chronic infections. the tests are specific for one virus.

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64
Q

what is EIA used for specifically

A

it can detect infections or vaccine efficacy

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65
Q

How do you test for viral antigens? what is the difference?

A

In ELIZA or EIA testing for viral antigens the tests actually tests for presence of virus in body. for viral ab tests the ab can be there long after infection is cleared.

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66
Q

lateral flow assay

A

viral antigen picks up virus specific gold labeled ab that is captured on strip

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67
Q

what is the accuracy of influenza testing

A

50-70% sensativity (pick up true positives) and 90-95% specificity (true negatives identified)

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68
Q

what are benefits to nucleic acid amplification tests?

A

High sensativites in the 90%. Use PCR.

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69
Q

How do NAAT work

A

Use PCR for DNA viruses and PCR with reverse transcriptase for RNA viruses to make DNA.

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70
Q

What are some advancements in NAAT

A

Isothermal tests- NSABA and LAMP

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71
Q

Describe NASBA

A

uses one temperature, only detects RNA, need sample RNA RT and RNA pol primers. used in HIV

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72
Q

What is the use for Real Time PCR

A

to determine viral load- amount of virus in sample, uses big or short probe with quencher. The greater the starting martial the faster fluoresence is detected.

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73
Q

Define incidence

A

The number of new cases of infection

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74
Q

Define prevalence

A

the total current cases of infection new and old per time

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75
Q

Define endemic

A

The base line level of disease in a community. the usual number of cases in a region

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76
Q

Define epidemic

A

An increase in the normal number of disease for a population. often sudden

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77
Q

Reasons for epidemics

A

1) an increase in the virulence or transmitibility of virus
2) intoduction to new population
3) increasing the exposure to population Ex: in water supply
4) increased susceptibly of host, aka low vaccine or immunity

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78
Q

define pandemic

A

an epidemic spread to other countries

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79
Q

What is R0

A

the total number of infected over the course of the disease on average. the avg amount of people infected from an infected person in SUSCEPTIBLE population

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80
Q

What is the formula for Attack rate?

A

calculated for an epidemic and gives %

AR= number of new cases in pop/population at risk

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81
Q

What is the formula for secondary attack rate?

A

2ndary AR= Number of contacts infected/total # of contacts

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82
Q

What is a communicable disease?

A

An infectious disease that is transmitted from one source to another. Includes contagious and non contagious diseases

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83
Q

Contagious is defined as what?

A

Contagious comes from the word contact, a very communinicable disease spread by contact or close proximity to an infected person, isolation could stop an epidemic of contagious disease

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84
Q

how are contagious diseases spread

A

Respiratory droplets, fecal oral, contact with skin abrasion is less common

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85
Q

What are non contagious diseases

A

Communicalbe diseases that are spread by more than casual contact. Needs needles sharing, sex, congenital transmission or by vector or perinatal shortly after birth (breastfeeding)

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86
Q

What factors increase transmissibility

A

1) longer survival outside the host
2) having an alternate host
3) Having a non human host that humans often contact
4) Port of entry ease, respiratory droplets>sex or blood
5) Ability to evade the immune system- replicating on mucosal surface first, mutating different strains
6) Having a long incubation may help. Person gets virus and doesn’t show symptoms but is infectious, ex: HIV. Incubation period is the time from infection to the start of sx
7) What route the virus is spread? Fecal oral is pretty efficient

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87
Q

What is the benefit to human to human transmission

A

No animal resoviour, easier to eradicate with vaccine

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88
Q

Zoonotic infections and arboviral transmission

A

Zoonnotic is animal to human, arboviral is insect to human- most of the time can’t be spread human to insect to human

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89
Q

Vertical transmission

A

parent to child, happens in germline for viruses. retroviruses in utero let transmission right after or during birth or in breast milk possible

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90
Q

Horizontal transmission

A

person to person

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91
Q

What diseases peak in winter and spring

A

Viruses that are enveloped and transmitted through the respiratory route- Influenza RSV and measles
Gastroenteric viruses- norovirus and rotavirus

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92
Q

What diseases peak in the summer and fall

A

enteroviruses in the picorna family and arboviruses peak in summer

93
Q

Is there a peak for STDs or blood viruses

A

nah

94
Q

Define incubation period

A

Time from infection until sx

95
Q

Define latent period

A

time from infection to virus is shed in body

96
Q

what is the primordial period

A

time from infection with generalized sx that are common to all infections before specific sx start
Ex; measles feel sick before rash

97
Q

What is the infectious phase

A

the that the infected person can spread the disease to others. can be infectious before sx arise. most of time stop being infectious prior to sx resolving. some people asx throughout infection

98
Q

what is the iceberg concept

A

when the number of asympomatic people with virus outnumber the ones who develop sx. asx can still spread disease

99
Q

what is infectivity

A

viruses ability to spread or infect individuals.

100
Q

what is pathogenecity

A

pathogenicity aka toxicity- the extent to which a overt disease is present in infected individuals. # of ppl with clinical disease/#infected. ABILITY TO CAUSE DISEASE

101
Q

Virulence

A

the extent of serious clinical disease present in infected individuals. # ppl with serious clinical disease/#infected

102
Q

How does age affect disease or infection

A

Young and old are at risk for serious complications. Poor immune response or acquired immunity in young and old. Some are worse in old people- Hep A VZV

103
Q

How do genetics influence disease susceptibility

A

mutuation in CCR5 makes people less susceptible to HIV, IL28B a INFgamma genes helps clear Hep C

104
Q

What are important things about local infections

A

It spreads on the surface of mucus membreanes in the organ but does not spread via the blood or lymph to different parts of the body. IgA is important. Can have short or long immunity. Incubation time is short. Targets skin, eyes, lungs, GI, respiratory tract. restricted by temp

105
Q

What is important about generalized infections

A

They enter the body and do not replicate at site of entry. Goes to lymph and to blood- viremia- then to large reticulendothelial organs and replicates- secondary viremia. now the virus to target organs. can be spread through nerves- rabies, HSV, VZV. longer incubation periods, 10 days to years, lead to lifelong immunity. IgG important. Rashes occur often

106
Q

Acute infections key characteristics

A

Most infections are acute and cleared by the immune system. Can lead to lifelong immunity to reinfection of same strain.

107
Q

Latent infections key characteristics

A

Are preceded by an acute infection. The virus lies dormant and does not replicate but periodic reactivation of virus occurs with reactivation of sx (HSV VZV).

108
Q

Chronic infections key characteristics

A

Are preceded by an acute phase where there is an early spike of virus the is reduced by the immune system. The initial spike is accompanied by primordial sx or subclinical. Can be long time no sx (HIV EBV HBV HCV HTLV) or can be asx for life.

109
Q

Slow infections

A

NOT proceded by acute infections or phase but a steady level of virus is present leading to disease many years after initial infection (usually decades). Slow infections are also chronic infections but with longer incubation period time to disease and lack of sx until disease

110
Q

What is the first line of defense to viruses? ex?

A

Physical barriers. Intact skin, mucous barrier, cilia, tears, low pH stomach and vagina

111
Q

Where are antimicrobial products secreted?

A

from the epithelial or MUCOSAL surface. SP-A and D MBL against glycoslayed proteins, B defensins against lipid env on HSV, SAP against influenza

112
Q

What is the main innate system defense against viruses and how is it triggered

A

Type I INF. Interferons are triggered by infected cells by patern recognition receptors on infected and neighboring cells. They can be produced by almost any type of cell upon infection.

113
Q

How do viruses avoid innate immune response? What is the counter by immune system

A

By shutting down type I INF by degrading proteins in the interferon pathway and avoiding pattern recognition receptors.

Plasmacytoid DC produce IFN without being productively infected so virus cannot shut down, pDC can produce large amount of IFN

114
Q

What is another playa in innate defense to viruses? When are they activated? How do they work?

A

NK cells are innate defense against viruses. They are activated by day two and kill infected cells in nonspecific innate manner or help clear adaptive response cells

115
Q

How are NK cells activated?

A

A balance between postive and negative activating signals

Postive- from receptors that recognize a variety of ligands that signal like MHC I that say cell is stressed or infected

Negative- binds lingands like MHC I that say cell is healthy and normal. Potent negative signal is receptor engagement of MHC I. Some viruses downreg MHC I on infected cells to keep from CTL killing but makes NK cells activated

116
Q

What is ADCC

A

Later in infection when ab response is active NK cells can kill infected cells that are coated by abs recognizing viral antigens expressed on the surface of the cell and FcgammaII receptor on NK cell. NEEDS viral antigen expressed on surface of cell

117
Q

What is macrophages role in viral protection

A

Innate and adpative immunity. They can phagocytize virus and dying infected cells. they produce NO TNF alpha and IFN. produce cheekiness and cytokines that help guide immune cells to site of infection and help NK cells survive. Very important in clearing body of infected cells

118
Q

What are DCs role in virus defense

A

Sample virus and activate PRP to produce IFN for non specific response. DC also produce cytokines and cheekiness that help guide the immune response to specific pathogens through activation of PRP.

119
Q

How can viruses start a systemic infection

A

by infecting DC or macrophages that travel to LN and tagging along and spreading to body

120
Q

Describe class switching in B cells to viruses

A

Ab response with B cells requires T cell Help CD4. The T cell signals determine the Ig isotope of ab. Antigens encountered in mucosal surface produce IgA primarily in MALT. Antigens in blood make IgG.

121
Q

What type of tissue produces IgA

A

In mucosa IgA dominates, made by IgA plasma blasts that also express a chemokine receptor that allows them to traffic to the respiratory tract and breast tissue that secrete chemokine specific to that receptor.

122
Q

Where is IgG made

A

In the blood, but some in mucosa (IgA primarily). In gut but much less in the upper respiratory tract where IgA dominates. More IgG in lower RT and Genitourinary tract

123
Q

What viral antigens are used in immune response

A

only the viral antigens on the surface of the virus are exposed to antibodies and are exposed. Infected cells only express antigens on the surface of the cell that would normally be on the surface of the virus

124
Q

what are the most important abs to virus protection

A

Neutralizing abs block the virus from infecting a cell. many viruses change their surface proteins to escape. still get CTL killing

125
Q

what are the role of CD8 CTL in virus defense

A

part of adaptive immune response. they recognize virally infected cells by presentation of viral proteins in MHC class I. they keep virus in check by killing infected cells. can kill any virus antigen presented on MHC I not just on the surface like neutralizing abs. Attack conserved “immunodominant” proteins in viruses

126
Q

why are you protected from reinfection by same virus strain

A

Long lived plasma b cells and secreted abs. the abs stay in mucosa and blood. Nuetralizing abs (IgA muc and IgG systemic) can bind to the virus and prevent infection and induce sterilizing immunity. better and higher abs from affinity maturuation and CTL memory response

127
Q

Why can you get sick from same virus again

A

IgA immunity doesn’t last past several years and wains- partial immunity, get sick but not as bad

128
Q

What is the life span of CTL memory response

A

memory CTL response helps clear an infection faster if cells are infected. In respiratory infections the memory is not long lived, only several years for influenza. CTL response is important in chronic infections though

129
Q

How can you get lifelong immunity/sterilization

A

from systemic infections like measles or chickenpox. IgG mediated in blood

130
Q

What 5 ways do viruses subvert the immune system

A

1) antigenic drift through mutations protect from neutralizing abs
2) latency- not producing virus. If reactivated CTLs can keep in check
3) Infecting immune priveldge sites yes brain testes. Ebola and zika
4) generalized immune suppression- measles, suppression for months or HIV destroys CD4 cells
5) specific immune suppression- reduce IFN I or reduce MHC I to escape CTL, produce mimics of cytokines like TNF receptor or ILIB to block cytokines from acting

131
Q

Describe a case of pathogenic CTL killing from virus infection

A

In liver infections with HBV and HBC it is the viral specific CTLs killing of infected cells that causes liver damage

132
Q

serum sickness

A

TIII HS, in HBV 1-10% with acute infection develop serum sickness

133
Q

Describe ab dependent enhancement in terms of Dengue virus

A

Dengue has four serotypes. Initial infection with one serotype creates neutralizing abs. If infected with another serotype the Nabs are present as bind virus weakly but not enough to neutralize. The ab coated viruses are taken up by macrophages enhancing the virus and leading to dengue hemorrhagic fever.

134
Q

Cytokine storm

A

excessive cytokine production d/t vigorous immune response leads to LUNG pathologies in resp infections

135
Q

goal of vaccines

A

to generate an immune response that protects against subsequent challenge with pathogen

136
Q

What makes a good pathogen to vaccinate against??

A

1) produce life long immunity from natural infections

2) not large number of strains

137
Q

what makes a hard pathogen to vaccinate against

A

lots of strains and changes season to season. Also not life long immunity (RSV) or produce chronic infections (HIV)

138
Q

what is most important in effective vacination

A

The ability of the vaccine to elect neutralizing abs

139
Q

What is the best vaccine method

A

Attenuated virues, few boosters needed, mimic natural infections and virus replicates in host, good ab and CTL response. Made version of virus that replicates but poorly in human. Are tested to make sure they don’t revert to pathogenic strain but small chance of getting infection ex: oral polio. Consider risk/benefit in immunocompromised patients

140
Q

What is the second best vaccine method

A

whole killed virus is 2nd best. requires large amounts of virus to be produced bc more material is needed in whole killed virus than attenuated. Need more innoculation than attenuated. No possibility for infection

141
Q

When is a subunit vaccine used

A

when virus cannot be grown in culture. Need adjuvant if subunit virus is used and might decrease dose in whole killed

142
Q

what adjuvants are used in vaccines

A

Alum causes antigens to aggregate boosting ab response. MPL is a detoxified version of LPS that is at least 1000 times less toxic than LPS- in Cervarix in HPV

143
Q

What vaccines do you need to pick proteins correctly?

A

only in subunit vaccines. WK and attenuated already have proteins for neutralizing ab response. Must pick antigen to elict neutralizing abs so must be on surface of virion

144
Q

MMR vaccine- type of vaccine, what is the dosing and response

A

Live attenuated vaccine, first dose at 12 months and second dose at 4-6 years, maternal IgG abs present in infect can prevent attenuated strain of virus from replicating making vaccine ineffective before age 1. Can be give at 6 months if going overseas

145
Q

What is herd immunity

A

Protection of whole community against an infectious agent by limiting the spread of infection. most people protected if large component of population can be immunized. Reduces the R value of virus

146
Q

what is passive immunity

A

Passive immunity is Ig transfer into a person. the protection is immediate but not long lived only weeks to months. active immunity takes weeks to develop but last a lifetime.

natural passive immunity- at birth from maternal abs that cross the placenta during the last trimester. majority is IgG that protect for months up to one year. Nursing prolongs passive immunity- colostrum is rich in ab. Breast milk has mostly IgA > IgG that protect for GI infection.

147
Q

when is passive immunity used that is not naturally occuring

A

used to prevent infection after potential exposure when no vaccine is present or indicated. or to prevent infection pre exposure in ab deficient disorders or RSV in premature infants

148
Q

What are Type I IFN produce? And where is receptor expressed

A

IFN I is IFN alpha and beta and others. Expressed on almost all cell types

149
Q

Where are type III IFN expressed and what type

A

IFN III = lambda, only expressed on epithelial cells, important in infections in mucosal cells- GI RT and liver

150
Q

What is the first thing triggered in viral infectioin

A

Pattern recognition receptors that recognize viruses turn on TF IRF3 and 7, makes IFN B which acts on infected and uninfected cells. IFN beta turns on IRF7 which activates IFN alpha and INF lambda 2-3 activated. pDC have IRF7 so make lots of IFN alpha quick- up to half of IFN in immune response from pDC without being productively infectected

151
Q

What does Type I and III IFN do?

A

They both turn on the same TF and so turn on same set of genes through STAT

Remember type III only on epithelial cells though

152
Q

What is the effects of interferons response genes? ISG

A

1) proteins turn off IFN signaling- IFN signaling is tightly regulated, downreg the receptor of turn off downstream signaling
2) Proteins in IFN pathway are upregulated, ampilifies the IFN signal and allows uninfected cells to be able to switch on IFN fast if infected
3) Antiviral genes- proteins that interfere with different stages of viral replicati

153
Q

How do you turn off IFN signaling

A

Remember genes ISGs code for proteins that regulate and turn off IFN signaling. USP18 binds to the receptor and prevents signaling from IFNalpha but still allows some IFNbeta signaling and IFN lambda signaling

CHC patients have upreg USP18

154
Q

What is IFN antiviral mechanism

A

IFN turns on the expression of OAS (oligoadenylate synthetase) but not active. If cells is virally infected OAS binds to viral dsRNA and is activated. OAS activates RNaseL which cleaves viral and cellular RNA.

155
Q

What is another antiviral of IFN

A

IFN turns on lots of genes that interfere with viral replication
Antiviral PKR- protein kinase RNA activated

Gene is turned on by IFN but is inactive, binding viral RNA turns on so that only infected cells activated PKR, activate NFKB, stops most protein systhesis!!! Stop cap dependent translation of proteins and some cap indep

156
Q

what are IFN effects on the immune system

A

1) increase antigen presentation and chemokine production
2) increase ab production
3) increase NK and CTL response to kill virally infected cells

157
Q

What is the role of half life in IFN therapy

A

IFN alpha has short half life, 3-8 hours so need 3 injections per week. If PEG then increase t1/2 and weekly injections

158
Q

What does IFN therapy treat

A

Tx for HBV HDV and some genotypes of HCV

Aleferon N for anogenital warts and resp papillomatosis

159
Q

What are some side effects of IFN therapy?

A

Within 8-24 hours- flu like sx but can resolve
BM suppression, granulocytopenia, thrombocytopenia
20-30% develop neuropysch side effects leads to DC in 10-16%

160
Q

what are some indicatioins for NSAIDs

A

Pain- decreases PGE2 which sensatizes nerves to bradykinin
Inflammation- inhibit COX and decrease PG
arthritis- pain and inflammation
Heachache, pain syndromes,
anti-pyretic- PGE2 increases temp in hypothalamus when activated by infection HS malignancy or inflammation, reset thermostat

161
Q

what levels do NSAIDs and glucocorticoids work

A

Glucocorticoids work upstream at phospholipase A2 preventing AA formation. NSAIDS block COX from making PG from AA

162
Q

How does NSAIDS block pain

A

by blocking COX can’t make AA to PGG-2 which is made to other PG and prostacyclin for pain

163
Q

Where is COX 1 and 2 found and expressed?

A

Cox1 is found in GI tract and constitutively expressed

COX2 is induced and found in the periphery

164
Q

what NSAID does not indiscreminately block COX 1 and 2

A

Celebrex only inhibits COX2 leading to less GI toxicity

165
Q

What NSAIDs slowly reversible bind to COX? and quicker

A

diclofenac flubiprofen indomethacin

Ibuprofen is quick and piroxicam and mef acid

166
Q

What are main NSAID cautions

A

Renal disease- deplete PGs and vasoconstrict afferent arteriole
Highly protein bound
monitor guiac stools- blood in stool from ulceration
Asthma- more leuktrienes
premature closure of DA from breast milk but also can close PDA

167
Q

How do NSAIDs lead to gastric ulcers following H pylori infection

A

they are acidic, they are anti platelet, decrease mucous production from dec PG production

168
Q

what are chronic overdose signs of NSAIDs

A

tinnitus, from increased AA,

also renal, bleeds, bruising are signs of too much too long

NSAIDs can raise BP increase Na retention,

169
Q

what is the triple whammy of renal blood flow

A

Glomerular bloodflow depends on BV which is dec by diuretics, PG which is impaired with NSAIDs, and angiotensin II which is impaired by ACE ihibitior

Can cause acute renal failure in elderly

170
Q

What are the roles of PGs made by COX1 and 2

A

Cox 1 PG- inhibit gastric acid secretion, stimulate GI mucus, maintain Renal bloodflow, enhance platelet aggregation

Cox2 PG- inflammation, (pain fever edema)

171
Q

What is REYES syndrome and what causes it

A

DO not USE ASA in children with varicella or flu sx

RS- acute brain damage and liver function problems that do not have a known cause

172
Q

What are highlighted side effects of ASA

A

Can increase serum UA levels and anatagonize gout drug. But can potentiate MTX. MUST BE DC at least 5 days before sx.

Can create HS reaction with bronchospasm and nasal obstruction mediated by cysttenyl leukotrienes

In asthma lipoxygenase is more active = more leukotrients

173
Q

ASA uses

A

at low does anti platelet, pyretic and angelic effect

high does - anti inflammatory so not used for that

174
Q

What is drug Ribarvirin used for?

A

Tx Hepatitis C but not used alone, inhaled (children) or oral for RSV, hematopoietic cell or heart/lung transplant in adults, hemorrhagic fever

175
Q

what is ribarvirin MOA

A

Inhibits IMPDH- results in a lower pools of guanine nucleotides to inhibit RNA and DNA viruses

176
Q

Ribavirin side effects?

A

major side effect of ribavirin is hemolytic anemia. increased levels of ribavirin in cells that they can’t rid causes RBC death

177
Q

Ribavirin in pregnancy

A

Nah. its is Category X teratogen. M and F birth control. health workers watch out for aersol form

178
Q

What polymerase inhibitors need to be activated by viral protein base analogues- HSV

A

Acyclovirs are pro drugs in nucleoside form that need phosphates added. The first is added by a viral kinase and the rest are added by cellular kinases. Only cells that are infected by HSV will be infected bc viral pol is more affected

179
Q

How does CMV activate drugs?

A

its uses Kinase UL97 to add first phosphate, most efficient for activation of ganciclovir

180
Q

Name the acyclovirs prodrugs and their active components and whats special for the three

A

1) Valcyclovir- active is acyclovir- most efficient chain terminator but short cell half life
2) Famiciclovir (oral)- active penciclovir (topical)- not obligate chain terminator but competitive inhibition of viral DNA pol. less potent but longer half life.
3) valganciclovir- active= ganciclovir, not obligate chain terminator but incorporation of several ganciclovir into DNA cause chain termination. More side side effects

181
Q

What is a drug that also acts against HSV but doesn’t need to be activated by viral kinases??

A

Cidofovir, can be used for viruses resistant to acyclovirs. also works against other DNA viruses

182
Q

What RT inhibitor does not need to be activated by cellular phosphorylation

A

Tenofovir- a nucleotide NRTI, do not need to be be activated by cellular phosphorylation

183
Q

What is the mechanism of action of NNRTI

A

bind a pocket in RT distal to active site and prevent RT. prevent forming active in RT.

184
Q

What is the MOA of foscarnet? what used to tx

A

it is an organic phosphatic acid that binds the phosphate binding site of pol and prevents nucleotide binding

used in Herpes and HIV-salvage therapy

185
Q

What is major dose limiting side effect of foscarnet

A

Nephrotoxicity

186
Q

What are the pol inhibitors used for HCV?

A

HCV inhibitors of NS5B pol ending in -buvir
blocks replication of viral RNA
sofosbuvir- nucleotide analogue and
dasabuvir is non nucleoside analogue

187
Q

what is the ending for HIV protease inhibitors

A

-navir

188
Q

Ending for HCV protease NS3/4A inhibitors

A

-previr, prevent polyprotein cleavage and thus replication

189
Q

what is the ending and MOA of NS5A HCV inhibitors

A

they inhibit binding of NS5A protein of HCV to reduce viral RNA levels and assembly and release of new virus.

end in asvir

190
Q

What are the name of HIV integrase inhibitors and what is MOA

A

Integrase inhibitors have tegavir in them

The integrates needs Mg cation, inhibitors chelate Mg active site

Also called INSTI

191
Q

What is MOA of maraviroc

A

it is an HIV entry inhibitor. It binds to CCR5 and prevents HIV envelope glycoprotein 120 from binding. If using CXCR4 as secondary receptor then ineffective

192
Q

Enfuvirtide (T20) fusion inhibitor MOA

A

blocks HIV envelope gp 41 from fusing viral membrane to plasma membrane. Mimics HR2 and binds to HR1 blocking entry

193
Q

what drugs prevent the infection of a cell vs. the spread of virus

A

Entry, RT and integrate prevent infection. Protease inhibitors prevent the production of infectious virus from an already infected cell.

194
Q

What is the uncoating inhibitor for influenza A? MOA side effects

A

Amantadine and rimantadine only influenza A
Amantadine has CNS and rimantidine has GI side effects
they bind to M2 protein of influenza A and prevent ion channel formation in endosome, no uncoating=no replication

195
Q

What are the budding inhbiitors of influenza? MOA and name

A

Neuraminidase inhibitors- amivir
works for A and B
neuraminidase cleaves off salic acid residues declumping and freeing virus to infect new cells. inhibit= tethered viruses and particles non infectious

196
Q

Do you treat HIV or HCV with one drug

A

no d/t drug resistance

197
Q

do you treat HBV with one drug

A

yes can be treated with tenofovir or entecavir that have little drug resistance. hard for HBV to mutate bc reg regions overlap DNA viral genes

198
Q

why do immunosuppressed people have more drug resistance

A

weak immune system leads to more replication of virus- higher chance of mutations, higher chance of resistance

199
Q

Why look at viral load

A

when to tx: HBV CMV

Efficacy of tx: HBV CMV HCV HIV

200
Q

how look at viral load

A

usually best is RT PCR for HIV HCV HBV CMV, if RNA virus must make cDNA first with RT

branch DNA- no amp, bind DNA or RNA (HIV HCV), not as sensitive as PT PCR

201
Q

When is genotypic testing used?

A

In HCV it is used to find subtype to tx differently

in HIV HCV HBV CMV genotype test for resistant viruses but a drawback is can only test for know resistance polymorphisms. there may be a new change that confers resistance not found in these tests.

202
Q

Describe HTLV1 vs 2

A

HTLV1 infects CD4> CD8. HTLV2 infects CD8>CD4

203
Q

What causes ATLL

A

HTLV1 in 2-5% of infections after 30-50years if infected before 20

204
Q

What causes HAM/TSP and what is sx

A

HTLV1 and 2 cause it by causing inflammation in the SC in 2-4% of cases after 4months to years. HAM sx= spasticity in legs with slow progression, no arm affected, some urinary problems

205
Q

Where is HTLV1 endenmic

A

Central africa, caribeean, south american parts, SW japan

in US more HTLV2 slightly, HTLV in US in indiginous people like Seminoles Navajo and Pueblo and with IV users 10-16%

206
Q

How is HTLV transmitted

A

Breast feeding (25% MAJOR WAY) but less if BF for 3-6 months, M-child is only 1:20 if no BF,

IV needle or transfusion, sex THROUGH INFECTED CELLS then clonally expands infected T cells. HARD TO FIND IN BLOOD SO NO BLOOD TRANSMISSION except in transfusion (85%) or needle use (10-16% of pop). CTL can keep in check but 5% develop ATLL

207
Q

What genes in HTLV involved

A

Tax initiates and HBZ sustains

208
Q

What histo finding in HTLV

A

Flower cells in ATLL

209
Q

What are the complications of HTLV1

A

2% develop HAM TSP tx with corticosteroids but 93% asx

210
Q

How do you detect HTLV

A

Ab ELISA test, Western blot to confirms

211
Q

What are the two important proteins in HIV

A

1) Gag is cleaved in matrix p17, capsid p24, and nucleocapsid p7
2) pol- cleaved in protease PR, reversere transcriptase RT, and integrase IN

212
Q

What are the other proteins in HIV

A

1) Tat- transcription activators can be excreted and increase expression of cellular genes
2) Nef- required for pathogenies- down reg MHC 1 CD 3 and CD4 and has SH3 down and can potentially activate cell signaling and excreted from infected cell
3) envelope glycoprotein precursor pg160 cleaved in p120 (receptor binding) and p41 (fusion of virus envelope with cell membrane)

213
Q

what does p120 bind

A

binds cd4, can be shed from infected cells, potential for binding CD4 on uninfected cells causing abberrant activation

214
Q

What are key characteristics of HIV2

A

Majority in west africa, lower levels of viremia, longer asx stage, slower decline of CD4 cells, difference in genes, resistant to NNRTI and enfuvirtide (fusion inhibitor), no protection to HIV1

215
Q

What are the key points of reverse transcription

A

Two strands of RNA- both the same
RT can bounce btn strands, how recombination occurs btw two strands/clades
**Proviral DNA has long terminal repeats needed to get into host genome, RNA does not have LTR, LTR contain many regulatory regions of HIV like promoters, polyadenation, transcription start site

216
Q

What leads to such high diversity in HIV

A

the high error rate of RT!!! more diverse than influenza world wide,

217
Q

what is goal of HIV tx

A

to get virus undetectable, 20-70 coopies/ml

218
Q

How are HIV designated by how they enter cells

A

Different designation based on chemokine receptor binding:

1) HIV that binds to CCR5 initially need high CD4 counts t infect- called macrophage tropic non syncia nducing
2) HIV that binds CRCX4 are called T cell tropic and syncia inducing
3) or dual tropic

219
Q

What co-receptors are expressed on which cells

A

CCR5 expressed on memory or activated CD4 T cells GALT macrophages DC microglia

CXCR4 is expressed on memory naivee resting CD T cells

220
Q

How do the co-receptors work for infection of HIV

A

Initial infection by CCR5 with high CD4, people will CCR5 deletion are protected from infection
over the course of infection the CXCR4 will present in a majority of infections with LOW CD4 counts

221
Q

How does for receptors effect rate to AIDS

A

If only have CCR5 still progress to AIDs but dual tropic progress faster

222
Q

Describe the acute infection of HIV

A

Initial infection by free virus of R5 strain through break in epithelium or DC/macrophage APC. A CD 4 T cells is infected or a macropahe with local replication for 3-4 days before the infected cells travel to the draining LN.

In days to weeks the virus goes to Lymph tissue and replicates high viral load. Immune system can reduce load but not clear the infection. Est the latent viral resouvir

223
Q

Where is an important place for HIV replication

A

GALT in gult in all stage of HIV. loss of th17 memory cells never recovers, less IL17 is less response, never gets better even with cART

disbosis and increased LPS in blood=continued immune activation

224
Q

How does HIV affect the brain

A

HIV can cross BBB or infected macrophages
infects microglia, perivas macrophages and sometimes astrocytes
without cART 20% develop demenita

225
Q

How does HIV progress

A

70% with flu like sx or mono with lymphadenopathy 2-4weeks after infection, initial level of virus is high, the more virus the worse off, 8-10 years to AIDs and95% die

226
Q

side effects of cART

A

increased risk of DM, CV diseases, bone fx, renal failure

227
Q

where does HIV hide

A

in resting memory CD4 cells, very low levels of replication in LN

228
Q

benefits of starting cART early

A

LN not destroyed, less GALT damage, less thymus loss, CD4 levels can be normal, lower co-morbidities

D/T 1 (3 decks)

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