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viro > virology exam 3 > Flashcards

virology exam 3 Flashcards

1
Q
  1. What structure does Picornavirus have? =
A
  • small, naked, icosahedral
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2
Q
  1. What is the genome of Picornavirus?
A
  • ss+RNA, linear and capped with VPg
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3
Q
  1. What are some medically important viruses of Picornavirus?
A
  • Rhinoviruses (common cold), Enteroviruses (Poliovirus & Coxsackie A and B), Heparnavirus/Hepatovirus (Hepatitis A)
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4
Q
  1. During replication of Picornavirus the whole genome is translated.
A

– P1 goes to VP1,2,3,4 (structural proteins) and P3 goes to polymerase and VPg

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5
Q
  1. What is the major protease during Picornavirus replication?
A
  • 3c (2a is also one)
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6
Q
  1. What is the polymerase used during Picornavirus replication?
A
  • 3D
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7
Q
  1. The plus sense (+ssRNA) of Picornavirus is?
A

– directly translated to polypeptide

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8
Q
  1. The negative sense of Picornavirus is?
A

– is the template to make more copies of plus sense; exits by lysis in intestinal cells

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9
Q
  1. How is Poliovirus transmitted?
A
  • fecal-oral transmission
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10
Q
  1. Are there still outbreaks of Poliovirus? =
A

– Yes. It has been eradicated from North America, but there are still outbreaks elsewhere in the world

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11
Q
  1. What does Poliovirus target in the paralytic form?
A
  • the anterior horn motor neurons
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12
Q
  1. What happens to intestinal cells and neuronal cells in the paralytic form of Poliovirus?
A
  • intestinal cells explode and come back, but neuronal cells explode and do come back so it is permanent paralysis (these neurons literally explode which do not regenerate and spinal cord damage is now permanent)
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13
Q
  1. Typical presentation of Polio:
A
  • asymptomatic, fever of unknown origin (FUO), meningitis, paralytic polio, and bulbar meningitis
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14
Q
  1. What are the symptoms of Paralytic Polio?
A

– fever and diarrhea; paralysis of one side of the body, usually legs before arms

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15
Q
  1. Paralytic polio can lead to?
A

– post polio

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16
Q
  1. What is Post-polio syndrome?
A

– inflammation of the spinal cord; partial paralysis’ paraplegic

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17
Q
  1. Post-polio can lead to?
A

– bulbar myelitis

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18
Q
  1. What is Bulbar myelitis?
A

– inflammation of the brainstem where neurons are killed and patient can’t walk, move arms, or no longer breathe unless with “iron lungs”

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19
Q
  1. What is the vaccine/treatment for Poliovirus?
A

– Dead Salk and Alive Sabin. Salk vaccine (killed) and Sabin vaccine (live, attenuated–no longer used in US)

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20
Q
  1. Salk vaccine - also called
A

inactivated polio vaccine (IPV); shot, killed vaccine

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21
Q
  1. Sabin vaccine - also called
A

oral polio vaccine (OPV); not a shot, originally was placed on a sugar cube

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22
Q
  1. What is the benefit of the Sabin vaccine?
A

provides the best immunity

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23
Q
  1. What is the problem with the Sabin vaccine?
A

because it is live attenuated it is able to replicate, hence causing paralysis

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24
Q
  1. What is the chance that the live, attenuated strain reverts back to original paralytic polio?
A

1 in one million

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25
Q
  1. What is the transmission of Coxsackie A & B?
A

fecal-oral

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26
Q
  1. What is the treatment/vaccine for Coxsackie A & B?
A

– no effective antiviral treatments, use handwashing for the best preventive mechanism

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27
Q
  1. Coxsackie A causes
A
  • meningitis, herpangina (red/white blisters back of mouth) & hand, foot, and mouth disease (Blisters on mouth hurt the most making it hard to eat)
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28
Q
  1. What strain of Coxsackie causes hand, foot, and mouth disease?
A
  • A 16
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29
Q
  1. What is the difference between Herpangina and Herpes?
A

– herpes is blisters on lips, gums, and tip of tongue whereas Herpangina is blisters on the back of throat and root of tonsils

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30
Q
  1. Coxsackie A 16 is typically seen in
A

babies; usually a little kid presents with a fever and gets blisters in 3 locations: palms, soles, and back of throat & tongue

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31
Q
  1. Coxsackie B causes:
A

meningitis, viral myocarditis, Bornholm’s disease (Devil’s grip)

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32
Q
  1. Viral Myocarditis is the number one cause of?
A

heart failure in patients under the age of 50 years old

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33
Q
  1. Bornholm’s disease (Devil’s grip) is what type of disease?
A

a respiratory disease/pulmonary infection breathe in horrible sharp pain in chest (feels like a piece of chest is being gripped)

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34
Q
  1. What is another name for Enterovirus 68 and 71?
A

Nonpolio Acute Paralysis Syndrome

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35
Q
  1. Enterovirus 68 and 71 are not?
A

– polio or coxsackie

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36
Q
  1. Enterovirus 68 and 71 were initially identified in?
A

1960s California, again in 2008-2009, 2010, 2015,2018

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37
Q
  1. Enterovirus 68 and 71 were typically seen in?
A

kids and caused paralysis

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38
Q
  1. What is the difference between paralytic polio and Enterovirus 68 and 71?
A

paralytic is paralysis of one side of the body and Enterovirus 68 and 71 paralysis is more widespread, progressive, and rapid

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39
Q
  1. What is the structure of Herpesvirus?
A

large, icosahedral, enveloped

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40
Q
  1. What is the genome of Herpesvirus?
A

linear dsDNA

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41
Q
  1. What does the tegument layer of Herpesvirus contain?
A
  • proteins that regulate host processes as well as early viral replication
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42
Q
  1. Where are the different places the envelope of Herpesvirus comes from?
A

first layer is from the nucleus, pulls from the plasma membrane, and also the ER; buds from nucleus, ER, Golgi/plasma membrane

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43
Q
  1. What family would a virus belong to if the envelope has been determined to contain nuclear proteins?
A

Herpesvirus

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44
Q
  1. Tegument is the layer between
A
  • nucleocapsid and actual virion to pack something inside of it
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45
Q
  1. How is Herpesvirus similar to Poxvirus?
A

large in structure, brings lots of things with it for replication, has its own DNA polymerase

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46
Q
  1. Herpes virus uses its own DNA polymerase. What is the benefit of the fact that Herpesvirus doesn’t hijack the host’s polymerase when it replicates in the nucleus?
A

We can make drugs that hurt the virus’ polymerase without hurting host polymerase

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47
Q
  1. How many different genome isomers of Herpesvirus is possible and why?
A

4; due to rearrangements around terminal and internal repeats on the long and short genome regions

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48
Q
  1. latency associated transcripts (LAT) allows the herpesvirus
A

to go latent until infection

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49
Q
  1. What is one thing that is true for all Herpesviruses?
A

Once you get a particular Herpes, you can have it for life (“the gift that keeps on giving”)

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50
Q
  1. What does Herpesvirus bind to get into the cell?
A
  • binds to extracellular matrix (heparans & chondroitin proteoglycans)
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51
Q
  1. concatemeric DNA is DNA that
A

is just copies of itself

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52
Q

What Are Gamma proteins

A

late proteins, structural proteins (nucleocapsid, glycoproteins etc.)

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53
Q
  1. During both productive and latent infection of herpes what is the shape of the genome?
A

–linear.

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54
Q
  1. Why does herpesvirus go through all these steps of immediate-early gene replications in productive infection?
A

– IE turns on E. E activates replication and forms concatemeric DNA, which is the template for L expression

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55
Q
  1. What happens to the viral DNA or herpesviridae during latent infection?
A
  • vDNA circularizes and is associated with host nucleosomes
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56
Q
  1. LAT latency associated transcripts is produced during latent infection and two things can happen ?
A

– RNA translated to protein called LAT protein OR RNA is maintained in nucleus: exons splice together: introns spliced out, but 1 maintains in RNA called the stable intron in Lariat configuration

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57
Q
  1. what is a lariat loop -
A

a loop formed when LAT mRNA is made

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58
Q
  1. Once the cell becomes permissive what occurs? –
A

reactivation, now active or productive infection

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59
Q
  1. What are some things that can cause herpesvirus to reactivate and go back to active infection? -
A

trauma to cell, hormone alterations, physiological stress, immunosuppression

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60
Q
  1. HSV1 is associated with? -
A

cold sore and gingivostomatitis (looks like herpanagina but is inflammatory condition of the gums inside the mouth)

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61
Q
  1. The initial infection of HSV1?
A

clinically unapparent

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62
Q
  1. Where does HSV1 lay dormant before reinfection?
A
  • trigeminal nerve root ganglia (retrograde, dynein)
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63
Q

Reactivation of HSV1 leads to?

A

classical vesicle formation on lips. “dew drop on a rose bud” serous-filled vesicle on an erythematous base (anterograde, kinesin)

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64
Q
  1. What is the vaccine and treatment for HSV 1? -
A

no vaccine; treated with Acyclovir and derivatives

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65
Q
  1. What percentage of time is a cold sore or oral presentation caused be HSV1?
A
  • 80%
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66
Q
  1. What percentage of the time is a cold sore or oral presentation caused by HSV2?
A
  • 20%
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67
Q
  1. HSV2 is associated with?
A

– genital herpes

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68
Q
  1. The initial infection of HSV2?
A

– clinically unapparent OR inflammation

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69
Q
  1. Where does HSV2 lay dormant before reinfection?
A
  • sacral nerve root ganglia (retrograde, dynein)
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70
Q
  1. Reactivation of HSV2 leads to?
A
  • classical vesicle formation on lips. “dew drop on a rose bud” serous-filled vesicle on an erythematous base (anterograde, kinesin)
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71
Q
  1. What is the vaccine and treatment for HSV2? -
A

no vaccine; treated with Acyclovir and derivatives

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72
Q
  1. What percentage of time is genital herpes is caused by HSV2?
A

80%

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73
Q
  1. What percentage of the time genital herpes is caused by HSV1? -
A

20%

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74
Q
  1. The initial infection of HHV3?
A

– chickenpox; technical name is varicella

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75
Q
  1. What makes chickenpox different from Poxvirus?
A

– asynchronous rash

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76
Q

39 What makes chickenpox different from measles or rubella?

A
  • Usually rash begins on chest or trunk and works its way out
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77
Q
  1. Reactivation of HHV3 leads to?
A
  • shingles, technical name zoster. With unilateral dermatome expression
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78
Q
  1. What is the vaccine and treatment for HHV3?
A

– live attenuated vaccine; treated with Acyclovir and derivatives in immunocompromised patients

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79
Q
  1. What percentage of people actually catch Herpes when patients shows no symptoms?
A
  • 70%
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80
Q
  1. Aseptic meningitis is the most common cause of –
A

viral meningitis and encephalitis and involves the temporal lobe

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81
Q
  1. Herpetic whitlow is due to-
A

touching herpetic sores

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82
Q
  1. Herpes gladiatorum is often associated with -
A

wrestlers using inoculated mats

83
Q
  1. Herpetic keratitis/ocular involvement leads to
A

– blindness in usually children

84
Q

Where does HHV3 lay dormant before reinfection?

A

in dorsal root nerve ganglia

85
Q
  1. HHV4 is associated with –
A

Epstein-Barr

86
Q
  1. What does HHV4/EBV infect and where does it go latent before reinfection?
A
  • the B-cells (entry via CD21) and can also act as a B-cell mitogen
87
Q
  1. In HHV4/EBV because B-cells proliferate leading to non-specific antibody response (heterophile antibody), what needs to happen?
A

T-cells need to control the infection

88
Q
  1. How many percent of us are exposed to HHV4 (EBV) as a child?
A
  • 95%
89
Q
  1. What is the clinical presentation of HHV4 if infected as a child?
A
  • clinically unapparent infection
90
Q
  1. What is the clinical presentation of HHV4 if exposed later?
A
  • tired, fatigue that can last for months, swollen lymph nodes, swollen spleen
91
Q
  1. What are you looking for when you perform a Monospot Test? -
A

looking for presence of heterophile antibodies

92
Q
  1. What are the multitudes of presentations that HHV4/EBV can present as in later reactivation? -
A

Burkitt’s Lymphoma, Nasopharyngeal carcinoma, Hodgkin’s lymphoma, Oral hairy leukoplakia

93
Q
  1. Burkitt’s Lymphoma in
A

Africa; a reactivation of HHV where lymph nodes in face start swelling, sometimes can knock teeth out and make it very difficult to eat; starts at the head; jaw dislocated and tonsils grow outwards

94
Q
  1. Nasopharyngeal carcinoma in
A

Asia; a reactivation of HHV/EBV; starts in nose and back of throat

95
Q
  1. Hodgkin’s lymphoma in
A

America; a reactivation of HHV/EBV; lymphoid on neck (can start in armpit or groin)

96
Q
  1. Oral hairy leukoplakia in
A

AIDS patients; a reactivation of HHV/EBV; white and hairy plaques present on the tongue & inside of mouth and cannot be scraped off

97
Q
  1. What is the treatment of HHV4/EBV? -
A

no vaccine, can use acyclovir in complicated cases but pretty rare

98
Q
  1. HHV5 is associated with -
A

Cytomegalovirus

99
Q
  1. The only difference between HHV5 from HHV4 is?
A

– HHV4 causes heterophile antibody positive infectious mononucleosis and HHV5 causes heterophile antibody negative infectious mononucleosis.

100
Q
  1. Where does the HHV5 virus go latent before reinfection? -
A

in B-cells

101
Q
  1. Cytomegalovirus can initially infect what and can cause what
A

– lymph nodes and salivary glands; pneumonitis

102
Q
  1. What can occur if exposed to HHV5/CMV during late uterine or early postnatal life? -
A

Cytomegalic inclusion disease of the newborn; can be life-threatening

103
Q
  1. HHV5 reactivation or representation is because of
A

– radiation/cancer, organ transplant, AIDS

104
Q
  1. In immunocompromised hosts, HHV5 reactivation can lead to what?
A
  • CMV retinitis which can lead to blindness; damaged liver; inflamed lungs
105
Q
  1. What is the problem with HHV5/CMV in women who are pregnant?
A
  • if never got exposed to it as a child, the initial infection can now cross the placenta, go to the baby and cause inclusion disease of the newborn & can kill the baby
106
Q
  1. Why can’t you give patients with HHV5/CMV acyclovir as a treatment?
A
  • does not encode thymidine kinase, so acyclovir is useless
107
Q
  1. What are the treatments for HHV5?
A

ganciclovir and derivatives, and foscarnet

108
Q
  1. HHV5/CMV has something called perinuclear halo
A

– described as owl eyes where there is a double nuclei associated with lungs (perinuclear halo is usually associated with HPV at the cervical level)

109
Q
  1. HHV6 and HHV7 are associated with –
A

roseola, 1 of the 5 rash-causing childhood diseases

110
Q
  1. What is roseola technically known as?
A
  • exanthem (erythema) subitum (“subtle rash”)
111
Q
  1. How is HHV6 &HHV 7 (roseola) characterized by?
A
  • a fever for a few days, followed by a faint rash that spreads from the trunk to the extremities
112
Q
  1. Where does HHV6 & HHV7 virus lay latent before reactivation?
A

in T-cells; may reactivate in transplant patients leading to bone marrow failure

113
Q
  1. What is the treatment and vaccine for HHV6 & HHV7?
A

no vaccine available; apparently can be treated with ganciclovir & derivatives (acyclovir useless because does not encode thymidine kinase)

114
Q
  1. HHV8 is associated with –
A

Kaposi’s sarcoma

115
Q
  1. What is Kaposi’s sarcoma?
A
  • a rare cancer in the general population, but relatively common in AIDs patients
116
Q
  1. Where does the primary and late infection occur for HHV8? -
A

in B-cells (no apparent disease); in tumor cells

117
Q
  1. What is the treatment for HHV8/KSHV? -
A

no specific treatment available, but reversal of immunosuppression often causes regression of the tumors (chemo & radiation if continues to grow)

118
Q
  1. Where did you hear of KSHV/Kasposi Sarcoma prior to late 1970s? -
A

in patients who were old men, who were usually Jewish & particularly in the Mediterranean area

119
Q
  1. For a long time Kasposi sarcoma was known as what? -
A

the “gay cancer” (essentially seen secondary to AIDS)

120
Q
  1. What is the clinical presentation of Kaposi’s sarcoma?
A
  • vascular bruises purplish-brown in color that can swell & get larger–not just on the skin: gums & tongues, rectum, in serious cases heart, liver, lungs
121
Q
  1. What are the divisions of why a patient could have Kaposi’s sarcoma? -
A

infected with AIDS, recent organ transplant, old Jewish guy, etc.

122
Q
  1. How likely is it for someone to contract HHV8/KSHV?
A
  • most people carry this virus but not clinically seen UNTIL you become immunocompromised
123
Q
  1. Which herpesviruses are usually transmitted through saliva & respiratory secretions?
A

3, 4, 5, 6, 7

124
Q
  1. Which herpesviruses are usually transmitted by direct contact?
A

1 & 2

125
Q
  1. What is the structure of Hepadnavirus?
A
  • enveloped, icosahedral/spherical
126
Q
  1. What is the genome of Hepadnavirus?
A
  • partial dsDNA/ partial –ssDNA (capped by nucleic acid)
127
Q
  1. What is the medically important virus of Hepadnavirus?
A
  • Hepatitis B
128
Q
  1. In Hepadnavirus, the virus overproduces?
A

– surface antigen (s, m, l) non-infectious polymers of surface antigens are found in blood during infection

129
Q
  1. In Hepadnavirus - fully-formed infectious particle of Hepatitis B (core DNA & surface proteins) is called -
A

“Dane particle”

130
Q
  1. How many open reading frames does Hepadnavirus have & what do they produce?
A
  • 4 open-reading frames produce 4 major proteins
131
Q
  1. PreC+C=?
A

E antigen

132
Q
  1. Pre-S2+S=? -
A

medium surface

133
Q
  1. Pre-S1+Pre-S2+S=?
A
  • large surface
134
Q
  1. X protein - regulatory protein -
A

associated with risk of cirrhosis/HCC

135
Q
  1. How does Hepadnavirus enter the cell and what is its target? -
A

enters by binding NTCP; target organ is the liver

136
Q
  1. When the genome of Hepadnavirus enter the nucleus what does the host do?
A

– elongates +DNA strand and creates covalently closed circular DNA (cccDNA)

137
Q
  1. When the genome of Hepadnavirus enter the nucleus what does your liver stop doing
A

– finishes copying DNA

138
Q
  1. In Hepadnavirus where does mRNA go for translation; surface proteins?
A

cytoplasm; mainly Golgi (can ER)

139
Q
  1. In Hepadnavirus host transcribes mRNA using –
A

DNA dep RNA poly

140
Q
  1. In Hepadnavirus after the host transcribes mRNA using DNA dep RNA poly, Full length mRNA is converted to –
A

DNA in cytoplasm via – viral polymerase (RT Activity)

141
Q
  1. In Hepadnavirus after the host transcribes mRNA using DNA dep RNA poly, Full length mRNA is converted to –DNA in cytoplasm via viral polymerase, DNA is then partially made –
A

double stranded by viral polymerase (DNA dep DNA poly activity)

142
Q
  1. How is Hepatitis B transmitted? -
A

exchange of blood, sexual contact, probably other body fluids

143
Q
  1. In Hepatitis B infected hepatocytes are targeted for –
A

destruction by CTL

144
Q
  1. How many percent of people clear the Hepatitis B infection if contracted as an adult? -
A

90-95% of adults

145
Q
  1. How many percent of people develop chronic Hepatitis B if contracted as an adult?
A
  • 5-10% of adults
146
Q
  1. How many percent of people clear the Hepatitis B infection if contracted during childhood? -
A

5-10%

147
Q
  1. How many percent of people develop chronic Hepatitis B if contracted during childhood? -
A

90-95%

148
Q
  1. Chronic hepatitis B: - increases
A

risk of liver cancer 100-150 fold

149
Q
  1. What is the prevention of Hepatitis B? -
A

a molecular vaccine (HBsAg);

150
Q
  1. What is the treatment of Hepatitis B for acute cases?
A

symptomatic treatment only

151
Q
  1. What is the treatment of Hepatitis B for chronic cases - antiviral medications are available pill:
A

Lamivudine, tenofovir, adefovir, (L,T 1st treatment A least effective) AND shot: PEGasys [interferon])

152
Q
  1. What is the problem with PEGasys, an injection of interferons, in patients with Hepatitis B? - common side effects are flu-like symptoms;
A

if have an auto immune disorder can’t take this medicine; in depression or mental illness, depression & suicide are relatively common

153
Q
  1. What is primarily used as a marker of infectivity in Hepatitis B?
A

HBeAg

154
Q
  1. What does “at risk” mean in terms of Hepatitis B?
A

someone who has never had Hepatitis B before and also has never been vaccinated before

155
Q
  1. HBsAg never infected, never vaccinated
A

susceptible so you should get vaccinated

156
Q
  1. HBeAg vaccinated –
A

protected against disease

157
Q
  1. Anti-HBes had infection before ad cleared it –
A

won’t get it again

158
Q
  1. Anti Core protein (IgM early and IgG late) has infection now –
A

tells about infectivity or contagious

159
Q
  1. Deltavirus is also known as: - “delta agent”
A

Deltavirus - the cause of hepatitis D

160
Q
  1. Why is Deltavirus known as a defective virus or a satellite virus?
A
  • because it requires hepatitis B for replication (does not encode its own surface antigen, steals HBsAg)
161
Q
  1. What is the structure of Deltavirus?
A
  • enveloped, icosahedral
162
Q
  1. What is the genome of Deltavirus? -
A

-ssRNA (but not contain its own polymerase)

163
Q
  1. What is the good thing about Hep D?
A

if you have been vaccinated against Hep B or had previous infection but cleared of Hep B, you cannot get Hep D (immune protection)

164
Q
  1. What is the initial shape of the genome of Deltavirus –
A

circularized with significant base pairing

165
Q
  1. Deltavirus: host RNA polymerase reads genome as dsDNA and then what is made –
A

mRNA which is used to make small D-antigen

166
Q
  1. Deltavirus: antigenomic RNA is made and is used as a template for genome production –
A

rolling strand formation, 85bp sequence functios as a ribozyme

167
Q
  1. When is the large antigen of Deltavirus produced – when host adenine deaminase ADA1 converts UAG stop codon to UCG serine;
A

increases length of small antigen by 19 AA; rewuired for viron assembly

168
Q
  1. What is the structure of Flaviviridae?
A
  • icosahedral, enveloped
169
Q
  1. What is the genome of Flaviviridae?
A

ss+RNA (some capped with nuclotide, some with VPa)

170
Q
  1. Major medically important viruses of Flaviviridae: -
A
  • Hepatitis C & Arboviruses
171
Q
  1. The whole genome of flavivirus is:
A

translated to form one polyprotein, which is then later cleaved

172
Q
  1. What is the initial part of the genome of flavivirus? -
A

structural proteins (C capsid, M membrane, E envelope proteins)

173
Q
  1. What is the latter part of the genome of flavivirus? -
A

non-structural proteins; NS3 is the important one (protease); when bound to others becomes helicase and RTPase

174
Q
  1. What is the function of NS4 – helper proteins
A
  1. NS4a is important for – NS3 to work

141. NS4b is important for – NS5 to work

175
Q
  1. What is the function of NS5 –
A

RNA dependent RNA polymerase

176
Q
  1. What protein is critical for attachment in Flavivirus? -
A

E-protein

177
Q
  1. How is Hepatitis C transmitted?
A
  • parental (blood mix) or sexual
178
Q
  1. What percent of Hep C cases progress to chronic hepatitis? -
A

80% of cases

179
Q
  1. What percent of cases of hepatocellular carcinoma is caused by Hepatitis C? -
A

25%

180
Q
  1. Why is Hepatitis C so hard to diagnose? -
A

because it is an acute infection, which is usually subclinical; never know you are sick

181
Q
  1. What basis is the diagnosis for Hepatitis C made? -
A

based on antibody against HCV; if positive a PCR is performed to determine if it is chronic

182
Q
  1. What percentage of patients with Hep C will develop cirrhosis? -
A

20% of patients

183
Q
  1. What is the treatment and vaccine for Hep C? -
A

no vaccine; treatment may include interferon and ribavirin combo; drugs maverick and harvoney

184
Q
  1. What is the difference between the ribavirin medication given to Hep C patients rather than in RSV patients? -
A

it is a pill

185
Q
  1. Telapravir - NS3 protease inhibitor;
A

75% chance of clearing the infection

186
Q
  1. Flavivirus (Hep C) eascapes Golgi by -
A

budding

187
Q
  1. What virus causes Hepatitis A? –
A

picornavirus; heparnavirus

188
Q
  1. How is Hepatitis A transmitted? -
A

fecal-oral transmission

189
Q
  1. What are the classic hepatitis symptoms caused by Hepatitis A? -
A

fever, malaise, anorexia, jaundice

190
Q
  1. How is Hepatitis A in healthy individuals compared to immunocompromised?
A
  • relatively mild, not chronic, no long-term complications; immunocompromised patients may have fulminant hepatitis
191
Q
  1. How is Hep A diagnosed? -
A

look at antibodies for IgM against HAV antigens

192
Q
  1. What is the treatment or vaccine for Hep A? -
A

both a killed & live vaccine are available & used in the US

193
Q
  1. What are the recommendations for the Hepatitis A vaccines?
A
  • for all children over 1 year old to get vaccine (been around only since early 2000s)
194
Q
  1. What is the structure of Hepeviridae? -
A

icosahedral, naked

195
Q
  1. What is the genome of Hepeviridae?
A
  • ss+RNA (capped by nucleic acid, not protein)
196
Q
  1. What is the medically important virus of Hepeviridae? -
A

Hepatitis E virus

197
Q
  1. What other virus did Hepeviridae used to be classified with?
A
  • Calicivirus (Norwalk virus); lytic infection
198
Q
  1. How is Hepatitis E transmitted?
A
  • fecal-oral transmission; often from contaminated drinking water
199
Q
  1. Hepatitis E: often asymptomatic, no chronic state; can lead to -
A

fulminant hepatitis in immunocompromised or pregnant patients

200
Q
  1. Where is Hepatitis E not common or not endemic?
A

U.S.

201
Q
  1. Where is Hepatitis E common?
A
  • Mexico, East Africa, & India have high prevalence
202
Q
  1. Where is hepatitis endemic?
A

– south America, mexico, central America

203
Q
  1. What is the treatment and prevention for Hepatitis E? -
A

no vaccine, no specific antiviral treatment available; ensure sanitary food & water sources, handwashing

204
Q
  1. If you had a patient with recent travel to Mexico who is pregnant, got a fever, turned yellow, & dropped dead, the most likely cause is? -
A

Hepatitis E

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