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DT4-Exam 1 > Viral STDs-Melissa*** > Flashcards

Viral STDs-Melissa*** Flashcards

1
Q

Human Papilloma Virus (polyomavirus):

Family, genome, capsid

A
  • Papovaviridae
  • Circular dsDNA
  • NOT Enveloped- NAKED!!, Icosahedral
  • NO BUDDING IN REPLICATION CYCLE BECAUSE THIS VIRUS IS NAKED!!
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2
Q

HSV:

Family, genome, capsid

A
  • Herpetoveridae
  • Linear dsDNA
  • Enveloped,Icosahedral
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3
Q

HIV:

Family, genome, capsid

A
  • Retroviridae
  • Linear ssRNA
  • Enveloped, Complex virus
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4
Q

Hepatitis B:

Family, genome, capsid

A
  • Hepadnaviridae
  • Circular, dsDNA
  • Enveloped, Icosahedral
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5
Q

Which 4 hepatitis viruses are sexually transmittable?

A
  • Hep C (flavivirus)
  • Hep D (Deltavirus)
  • Hep A (Picornavirus)
  • Hep B (Hepadnaviridae)

**Note that E is only fecal-oral

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6
Q

Molluscum contagiosum is caused by which virus?

When is this sexually transmittable?

A

Poxvirus infection; sexually transmittable in immunosuppressed patients

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7
Q

List two Herpetoviridae viruses other than HSV that can be transmitted sexually:

A
  • CMV

- HHV8 (Kaposi sarcoma virus)

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8
Q

List one retrovirus other than HIV that can be sexually transmitted:

A

-Human T cell leukemia Virus 1

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9
Q

List 4 factors that come into play when determining whether or not patient will become infected from sexually transmitted virus:

A
  • virulence of the virus (varying antigenicity?)
  • status of immune system
  • genetics (expression of receptors for virus)
  • pre-exisisting lesions?
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10
Q

What are two factors that make immune defense against STIs difficult?

A
  • alteration of antigenicity (i.e. HIV: gp120, gp41, p24)

- existence as multiple serotypes/ genotypes

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11
Q

SV40:
Which family is it in?
What two infections can it cause?

A

Papovaviridae

  • Lytic infection
  • Transformation
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12
Q

Describe the events of a lytic SV40 infection

+ Which cells does this occur in?

A

In permissive cells…(that allow replication)

Early:
Viral DNA–> early mRNA–> early proteins (T/t- antigens)

Late:
T antigens bind viral DNA–> genomic replication initiated–> Late mRNA–> late (structural) proteins–> virus assembly–> host cell LYSIS w/o budding

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13
Q

Describe the events of SV40 induced cell transformation:

+ what cells allow this infection?

A
  • NONPERMISSIVE cells that are NOT capable of replicaiton:
  • ONLY EARLY events occur: early mRNA–> T, t Ags
  • T, t Antigens bind cell DNA–> TRANSFORMATION INSTEAD OF REPLICATION!!!!
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14
Q

What happens to a cell when it transforms– what is lost/ gained?

A
  • Lose contact inhibition
  • Replicate w lower growth factor requirement
    =tumor formation
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15
Q

List 3 papovaviruses that cause human disease:

A
  • JC Virus: Progressive Multifocal Leukencephalopathy
  • BK Virus: Hemorrhagic cystitis
  • HPV: skin/ mucosal infection WITHOUT viremia

If you eat at Burger King God will punish you with bloody peeee🍔🍟

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16
Q

What are the 4 HPV viruses that can infect the anogenital tract?
What are the two modes of transmission?

A

HPV 6, 11, 16, 18

  • sexual transmission
  • direct contact with infected skin
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17
Q

Which layer of the skin does the HPV virus infect? In what cells does it replicate?

A

Basal layer infection (immature cells)–> Squamification / Keritiniization–> replication in mature cells to form papillomas and warts

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18
Q

What are the 4 morphologies of HPV infection?

Which can become cancerous cells?

A
  • Filiform (fibrous protrusion)
  • Flattened (plantar wart)
  • Cauliflower like (condyloma/ genital wart)
  • Dysplasia (cervix)

Skin + genital papillomas; cervical dysplasia–> ~cancer, esp with sun exposure (NAKED SUNBATHING?)

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19
Q

Where does HPV DNA remain latent?

A
  • latent in basal layer of skin and mucosa

- immunocompromise–> reactivation of infection

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20
Q

How do we treat skin papilloma/ dysplasia?

A
  • podophyllin from mandrake plant applied topically (rare)

- more commonly laser or surgical removal

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21
Q

Describe the characeristics of the HPV (QHPVV) vaccine:

  • What is the valence?
  • what is the antigen?
  • what is the vector?
A
  • Quadravalent: L1 from 6, 11, 16, 18 + Al adjuvent
  • HPVL1 protein (capsid protein)
  • Yeast vector
  • Patient will have immunity to 4 strains and possibly others
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22
Q

How is the QHPVV administered? When?

A

IM over 3 dose schedule (0. 2. 6 mos) between 11-12yoa (must be 9+yoa)

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23
Q

How do we test for HPV?

A
  • NO SEROLOGY testing (cant grow in tissue culture)

- Use nucelic acid bases analysis (PCR)

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24
Q

Primary mode of HIV transmission in undeveloped countries vs. developed countries:

A
  • undeveloped countries: heterosexual sex

- developed countries: MSM sex

25
Q

Factors that increase HIV prevalence in developing countries?
Why are the rates ^^ in Asia/ Africa?

A
  • Preexisting STIs like syphilis chancres= route for infxn

- Asian and African strains have greater affinity for genital mucosal cells

26
Q

4 factors increasing risk of HIV infection:

A
  • uncircumcised males

+ sketchy things: anal intercourse, multiple partners, promiscuous, unprotected sex

27
Q

What is the HBV Dane particle?

A

core structure surrounded by envelope

28
Q

HBV: What is the primary core particle? envelope particle? which is the particle that confers infectivity?

A
  • HbcAg = core antigen
  • HbsAg= surface antigen
  • HbeAg = infectivity
29
Q

How is HBV transmitted?

A

Blood, sex, transplacental

30
Q

From where do herpesviruses acquire their envelope?

Where/ how do they replicate?

A

nuclear budding/replication, rolling circle/ concatemer replication

31
Q

Describe how HSV2 infection occurs:

A

incubation 3-7days–> ulcers + regional lymph node swelling + flu sx.

Lesions heal in 2 weeks; virus latent in sacral ganglia

32
Q

How do we dx and tx HSV infection?

A

Dx: specific Ab + immunofluorescence (HSV 1 vs 2)

Tx: Acyclovir (can be given prodromal too), Valacyclovir, Famiclorvir

33
Q

In what family is the Zika virus?
Describe the genome + structure
What is the vector for infection and where is it endemic?

A

-Flaviviridae
(+ ssRNA; icosahedral, enveloped)
Aedes aegypti/ albopictus Mosquitoes
Endemic in South America, especially Brazil

34
Q

What kind of infection can the Zika virus cause?

viremia?

A
  • 80% limited disease
  • Pregnant woman can have fetal defects/ microcephaly
  • Guillan Barre Syndrome (suggests viremia)
35
Q

When do the mosquitoes carrying zika virus lay their eggs?

A

Lay eggs in dry season–> dormant for 4 mos–> exposure to rain–> larvae w zika

36
Q

List the viruses that can cause congenital infection due to reactivation in mother (4)

A

Polyomavirus
CMV, EBV
HSV 2, 1

37
Q

List the viruses that can cause primary infections in mothers and their fetuses (3)

A

-Rubella
-Zika virus
-Parvo B19
(viruses from this lecture)

++ HIV, CMV, VZV, HSV, HBV (Classic DNA viruses)

38
Q

Rubella Virus:
Family, genome, structure
Describe course of virus

A
  • Togavirus (NOT an arbovirus!)
  • (+) ssRNA
  • Icosahedral, enveloped w/ spikes
  • starts as URI–> 2-3 wk incubation –> viremia (rash, nodes, congenital rubella syndrome)
39
Q

Describe the typical adult/ child infection caused by rubella virus. What type of infection might it cause in women?

A
  • Many have inapparent infection
  • URI, 3 day rash from face to limbs, PERIAURICULAR LYMPHADENOPATHY
  • Arthritis in females
40
Q

Congeital Rubella syndrome:

  • When does it occur?
  • How does the disease cause infection?
  • What are six possible sx/ sequelae?
A
  • first trimester (1st month = most severe)
    -CHROMOSOMAL DAMAGE (not lytic) –>
    PREVENTS NORMAL TISSUE GROWTH–>
    Mental retardation, cataracts, deafness, HSmegaly, possible Guillian Barre or death
41
Q

How long are children with congenital rubella infectious to others?
How and when do they transmit virus?
How do we dx?

A
  • secrete virus for 2 years
  • source of infection to others via nasal secretions and urine, usually in the spring
  • 4x rise IgM
42
Q

Which strains of rubella virus are covered by the rubella vaccine? (2)
What type of vaccine is it?

A
  • RA 27-3
  • Cendehill
  • Vaccine is LIVE ATTENUATED; recommended not to use on preggos, but “accidentally” found to be safe…
43
Q

What are the two target populations for vaccination against rubella? Possible ADRs? What is the valence of the vaccine?

A
  • Women of childbearing age
  • Kiddos under 12 mos (reservoir for infection)
    -allergic reaction to neomycin, arthritis in females like the virus
    -Trivalent vaccine covering measles, mumps, and rubella
    (Quadrivalent including varicella is available)
44
Q

Dependovirus:
Family, genome, structure?
Can this virus cause human infection?
How does it replicate?

A
  • Parvovirdae
  • ssDNA
  • small, naked, 3 protein-icosahedral capsid

*This is an incomplete virus that requires adenovirus or HSV to replicate; it can not cause human infection

45
Q

Erythrovirus/ Parvovirus B19:

Family, genome, structure?

A
  • Parvovirdae
  • ssDNA
  • small, NO ENVELOPE, 3 protein-icosahedral capsid
46
Q

Describe the unique requirements for parvovirus replication:

Why is it common in babies?

A
  • Small genome–>
  • Requires ACTIVELY DIVIDING cells to infect; can not carry its own machinery
  • Common fetal/ newborn infection because these guys have rapidly dividing cells
47
Q

What are the 2 non-structural proteins coded for by parvovirus genome? What is their function?

A

NS1, NS2 –> promote replication cycle

48
Q

What type childhood disease is caused by Erythrovirus/ Parvovirus B19? How does it present?

A

“Fifth Disease” or Erythema infectiosum

- “slapped cheek” MP rash

49
Q

How is erythrovirus/ parvovirus B19 transmitted?
What kind of disease might it cause in the event of congenital infection?
What is one factor that influences the severity of outcome in congenital infection?

A
  • Respiratory droplets
  • Primary infection of mother–> Congenital infection–> Death in utero or blood stuff (HSM/ anemia/ hydrops fetalis)
  • Worse outcome with infection during early gestational age
50
Q

How do we test for erythrovirus/ parvo B19?

How much of the population is immunized?

A

Specific IgM or PCR

50% of population unknowingly immunized

51
Q

What are the two ways that CMV could cause congenital infection?
Which causes fetal abnormalities?
Is there a time in gestation when infections are worse?

A
  • primary infection of the mother
    (more common, difficult to dx because typically asx)
  • reactivation of latent infection in LATE preggos
    (rare, WILL NOT LEAD TO FETAL ABNORMALITIES)

*worse infection not associated with gestational age

52
Q

What is one factor associated with frequency of congenital infection?

A

Lower maternal T cell response to CMV Ags –>

^ rate fetal infection

53
Q

What are some of the problems caused by congenital CMV infection (4)?

A

3 neuro, 2 heme

  • CNS; Auditory/ Vision loss
  • HSM; Thrombocytopenia purpura
54
Q

VSV: family and genome?

A
  • herpetoviridae (like CMV, Herpes)

- dsDNA

55
Q

Under what circumstances can VSV cause congenital infection and what is the outcome of such infection?

A
  • primary maternal infection during first trimester
  • causes limb, muscle, nerve defects

*note that congenital infection due to reactivation is rare and infants can acquire the infection perinatally during partuition

56
Q

How do we prevent congenital HIV infection?

What kind of virus is HIV?

A
  • +SSRNA, retrovirdae
  • HAART heavy in last trimester to decrease viral load
  • c- section, no breastfeeding
57
Q

What are some of the consequences of congenital HIV infection? (5)

A
  • low birth weight
  • pneumonitis
  • thrush
  • HSM + diarrhea
  • CNS damage
    (same as HIV in adults basically!!)
58
Q

HBV structure and family:

What are the three ways that HBV can cause congenital/ neonatal infection?

A

Hepadnavirdae: partial dsDNA

  • primary infection during preggos
  • chronic active HBV infection w ^ HbeAg
  • perinatally during partuition
59
Q

How do we treat HBV in infants with congenital or perinatally transmitted HBV?

A
  • pegylated IFN + antiHBV drugs
  • IMMEDIATE vaccination of ALL babies w/ HBV+ mothers
  • Hyper Anti-HBV-Ig

DT4-Exam 1 (17 decks)

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