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Viruses > DNA Viruses > Flashcards

DNA Viruses Flashcards

1
Q

List the DNA Viruses (11)

A 
HSV (1,2)
EBV
CMV
VZV
HHV (6, 8)
Polyomavirus (JC, BK)
HPV (6, 11, 16, 18, 31, 33)
Parvovirus 
Adenovirus 
Pox Virus
Hepatitis B
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2
Q

HSV 1 and HSV 2 transmission

A

Sex, saliva, vertical (TORCH)

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3
Q

How can you visually recognize HSV 1 and HSV 2?

A

Intracellular inclusion bodies - Cowdry bodies

Host cells with big, target-like eosinophilic bodies in the nucleus

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4
Q

Which viruses are part of the herpes virus family? (7)

A 
HSV 1 (HHV 1)
HSV 2 (HHV 2)
VZV (HHV 3)
EBV (HHV 4)
CMV (HHV 5)
HHV 6 (Roseola and Herpes Lymphotropic Virus)
HHV 8 (Kaposi Sarcoma)
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5
Q

All about HSV-1 (8 points)

A

1) Usually confined to upper half of body
2) Usually first presents as gingivo-stomatitis (more often in infants). This is widespread inflammation of lips and gums. Eventually this just turns into cold sores - herpes labialis.
3) Also causes keratoconjunctivitis - serious eye infection that you should see an ophthalmologist for - They will use a Fluoroscein slit lamp exam to reveal serpiginous corneal ulcers.
4) Also associated with temporal lobe encephalitis - causes hemorrhage and necrosis of inferior and medial temporal lobes.

Fever, HA, seizure, altered mental status

Unique to herpes encephalitis:

Bizarre behavior and olfactory hallucinations - also personality changes

5) HSV-1 remains latent in trigeminal ganglia - reactivated by stress or immunocompromise
6) Herpes rash has “dew drops on rose petal” appearance - clear vesicles on erythematous base
7) Herpes on the fingers is Herpetic Whitlow - more common in dentists (caused by HSV1 and 2)
8) Another derm note that is more common in 1 than in 2 is erythema multiforme

Hypersensitivity rxn that causes small target lesions, usually on baks of hands and feet that then move in centrally

Seen 1-2 weeks after infection

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6
Q

What is the most common viral infection of the mouth?

A

HSV-1

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7
Q

What is the most common cause of sporadic encephalitis in USA?

A

HSV-1

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8
Q

All about HSV-2 (6 points)

A

1) More down below
2) Sex, obstetrics
3) Causes herpes genitalis - painful inguinal lymphadenopathy with clusters of vesicles with a red bases

Def painful and vesicular

4) Latent in sacral ganglia
5) Can cause aseptic meningitis in adolescents and adults
6) PCR is test of choice for dx, but before PCR you’d scrape ulcer base and perform Tzank Smear

Smear would show multinucleated giant cells characteristic of herpes infection

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9
Q

HSV-1/HSV-2 Tx

A

No cure - have it for rest of your life

To prevent breakouts:

Acyclovir
Valcyclovir

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10
Q

What disease is caused by EBV?

A

Infectious mononucleosis

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11
Q

EBV transmission

A

Saliva - sharing drinks to kisses

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12
Q

EBV symptoms

A

Fever
Tender lymphadenopathy (normally posterior cervical region, can be generalized)
Splenomegaly
Pharyngitis (tonsilar exudate)

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13
Q

EBV pathogenesis

A

On blood smear, you will see a reactive lymphocytosis - Reactive cytotoxic CD8+ T cells (Downey or atypical cells)

Atypical lymphocytes are mostly CD8+ cytotoxic T cells, but they can also be NK cells.

In response to infection, T cells proliferate causing lymph node and spleen enlargement

When virus gets in new host it targets B-lymphocytes (WBCs that turn into plasma cells and make antibodies or remain dormant waiting to make antibodies in response to another infection)

EBV remains latent in B cells

To infect the B cells, the EBV envelope glycoprotein binds to CD21 (receptor for complement component C3d)

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14
Q

How do you differentiate Mononucleosis from Strep pharyngitis?

A 
Strep = kids, adolescents 
Mono = asymptomatic at young age, symptoms in late teens, adults

Patient presents to doctor with severe sore throat. Doctor suspects strep pharyngitis and gives amoxycillin. Patients with mono who get treated with amoxycillin or ampicillin develop a maculopapular rash (NOT an allergic rxn)

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15
Q

What diseases or people with EBV more at risk of developing?

A

In patients with weakened immune systems, EBV is associated with higher risk of developing 2 types of B Cell lymphoma:

1) Hodgkin Lymphoma - Reed Sternberg cells look like owl’s eyes

Mixed Cellularity Subtype - EBV seen in 70%

2) Non-Hodgkin Lymphoma - Burkitt Lymphoma

Endemic/African Burkitt Lymphoma presents with large jaw lesion and swelling

Sporadic Burkitt develops in ileosecal or in peritoneum

t8;14 translocation

Also, Asians are at higher risk for developing Nasopharyngeal Carcinoma

EBV is also associated with oral hairy leukoplakia:

This is most often seen in Pts with HIV
It is not a precancerous lesion
It does not develop into Squamous cell carcinoma
The lesions are on lateral portions of the tongue and may look like Candida (Candida can be scraped off though)

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16
Q

How do you diagnose EBV?

A

During acute infection, EBV activates B cells to secrete heterophile anti-sheep RBC antibodies. The presence of these antibodies is used to make diagnosis of mono as they will agglutinate sheep or horse RBCs

Monospot Test - rapid diagnosis in clinic (IgM)

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17
Q

Treatment for EBV

A

mostly supportive

Tell patients they must avoid all contact sports due to the risk of splenic rupture. Splenomegaly is in 50-60% of Mono patients.

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18
Q

What are some common features among the herpes viruses?

A

Remain latent in cells

Replicate in nucleus

DNA

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19
Q

Where is CMV latent?

A

mononuclear cells (WBCs with 1 nucleus)

  • Lymphocytes (B & T), monocytes, macrophages
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20
Q

CMV transmission

A 
Blood
Breast milk
Sexual contact
Saliva
Urine
Vertical (TORCH)
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21
Q

Who is most susceptible to CMV?

A

CMV becomes reactivated during immunosuppresion

  • Transplant patients on immunosuppresants as well as patients with HIV/AIDS
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22
Q

What is the most common fetal viral infection?

A

CMV

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23
Q

What is the #1 cause of mental retardation due to congenital viral infection?

A

CMV

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24
Q

Congenital CMV presentation

A

Blueberry muffin rash - can cause thrombocytopenia (presents clinically with petechial rash) - the same rash that’s in congenital rubella

Jaundice and hepatosplenomegaly

Sensorineural deafness

Structural abnormalities in the brain:

  • intracranial calcifications (periventricular calcifications - around the ventricles, seen in toxoplasmosis too)
  • ventriculomegaly
  • Changes in brain structure lead to mental retardation or seizures

80- 90% of newborns who get congenital CMV are asymptomatic, but 15% of these lucky ones go on to experience some hearing loss so routine screenings are still important.

Second trimester is associated with highest risk of congenital CMV in an infected pregnant mother

Another presentation:

Hydrops fetalis - heart failure leading to severe edema and fluid accumulation in multiple compartments of the fetus that most often leads to spontaneous abortion.

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25
Q

What is the #1 cause of sensorineural hearing loss in children?

A

CMV

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26
Q

CMV in transplant patients

A

Immunosuppressed

At risk of developing CMV pneumonia

To detect CMV in transplant patients, perform a Buffy Coat Culture

Buffycoat is part of blood that contains WBCs and platelets. Incubate these cells with Fluorescent Anti-CMV Antibodies and detect presence of the virus

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27
Q

CMV in AIDS patients

A

Immunosuppressed

AIDS patients are especially susceptible to CMV infection when CD4

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28
Q

What do cells infected by CMV look like?

A

You’ll see Owl’s Eye inclusion bodies

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29
Q

CMV Tx

A

1st line = ganciclovir

2nd line = Foscarnet - used when virus has UL97 gene mutation that makes it resistant to ganciclovir

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30
Q

CMV infection in adults who are not immunosuppressed

A

It is possible

Most common presentation is CMV Mononucleosis

Same symptoms as EBV mono (sore throat, lymphadenopathy, fatigue) but it is Monospot (-) on a pharyngeal swab.

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31
Q

What disease is caused by Varicella Zoster (VZV)?

A

Chicken pox

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32
Q

Chicken pox transmission

A

Respiratory transmission

or from ruptured vesicles themselves

Can have vertical transmission of VZV (TORCH)

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33
Q

Chicken pox presentation

A

from VZV

One of the childhood exanthams

Fever, HA

“Dew drops on a rose” rash - a vesicular lesion with surrounding erythema

Lesions will be in different stages of healing (some blisters, some healing scabs) - In smallpox it’s very similar but the lesions are all at the same stage

Tzank Smear shows multinucleated giant cells (can be HSV or VZV)

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34
Q

Serious complications of chicken pox

A

Adults with chicken pox are more likely to develop pneumonia or encephalitis (esp the immunocompromised)

Pneumonia and encephalitis can happen in kids with VZV too, but adults who are immunocompromised are at much higher risk.

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35
Q

Varicella vaccine

A

Live, attenuated for children

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36
Q

Chicken pox Tx

A

Acyclovir for kids 12+, adults, immunocompromised

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37
Q

VZV latency

A

VZV remains latent in nerves (specifically dorsal root ganglia)

When people are under stress or are immunocompromised VZV can reactivate - usually in older people or immunocompromised

When it becomes reactivated it has 2 names: Herpes Zoster or Shingles

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38
Q

Shingles/Herpes Zoster presentation

A

Shingles has “Dew drops on a rose” appearance with a characteristic dermatomal distribution

From Dorsal root ganglia, VZV travels down sensory nerve fibers to skin (hence the dermatomes)

Usually lumbar and thoracic dermatomes

Rarely crosses midline

If it does cross the midline, we have disseminated VZV and is a RED FLAG for immunocompromised (if there is no history of chemo…test for HIV… something must be going on)

The rash is extremely painful. Even when rash goes away, you can still have pain in a dermatomal distribution (Post-herpetic neuralgia)

Normally thoracic dermatomes, but sometimes it an affect the trigeminal nerve, esp in immunocompromised hosts. Can lose vision (V1 affected) - Herpes Zoster Opthalmicus

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39
Q

Herpes Zoster vaccine

A

Zoster vaccine

Live attenuated

Recommended for adults > 60. Don’t give it to people who are actively immunocompromised (pregnant women, leukemia/lymphoma)

Can still give to HIV patients if CD4 > 200

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40
Q

Shingles Tx

A

Acyclovir

Famcyclovir (easier to dose)

Valcyclovir

41
Q

Congenital VZV

A

TORCH

If pregnant woman gets VZV during Trimesters 1-2, the child can develop Congenital Varicella Syndrome:

Limb hypoplasia
Cutaneous dermatomal scarring
Blindness

42
Q

What disease is caused by HHV-6?

A

Roseola (Sixth Disease), AKA Exanthema Subitum

43
Q

What cells does HHV-6 infect?

A

CD4+ Helper T Cells - it can cause immunosuppression by killing off these cells

44
Q

Roseola symptoms

A

HHV-6 (Exanthema Subitum)

Primarily in children 6 months - 2 years old

High Fever that lasts 3-4 days - can sometimes be high enough to cause seizures ( > 104 for seizures)

The fever is followed by macular rash (diffuse except face) - lacy appearance, spares face

Timing is very important: Fever is 4 days THEN as fever subsides the rash appears

Roseola is usually self-limiting

Tx is supportive (no FDA approved Tx) with cooling measures and adequate fluids

45
Q

How do you differentiate Roseola from Measles?

A

Measles does NOT spare the face
Roseola does spare the face

Measles has simultaneous fever and rash
Roseola has fever THEN rash

46
Q

What disease does HHV-8 cause?

A

Kaposi Sarcoma (an AIDS-defining illness)

47
Q

HHV-8 transmission

A

Sexual contact (including kissing) especially in men who have sex with men

48
Q

What 3 populations are most at risk for Kaposi sarcoma?

A

1) AIDS/immunocompromised
2) Elderly Russian men (present with lower extremity lesions)
3) People in areas of Africa where virus is endemic (the classic palatal lesions in adults, can be fatal in kids)

49
Q

Kaposi Sarcoma presentation

A

Erythematous violaceous lesions on nose, extremities, and mucous membranes.

Lesions arise from primitive vasculature forming mesencymal cells. Newly created blood vessels (angiogenesis) within the lesions cause the purple color - REMEMBER - the color is from the proliferation of vasculature.

The virus accomplishes this vasculature proliferation through the dysregulation of VEGF resulting in angiogenesis

Lesions can occur on mucosal surfaces as well (ANYWHERE along GI tract - you can see on colonoscopy).

Most common location of these plaques is hard palate

HHV-8 can also infect B-cells and cause Primary Effusion Lymphoma (a B-cell lymphoma)

50
Q

How do you differentiate Kaposi sarcoma from Bacillary Angiomatosis

A

Kaposi lesions look like many others

Bacillary Angiomatosis is from Bartonella.

Examine the lesion microscopically to tell them apart

Kaposi: seen with lymphatic infiltrate (viral etiology)
Bacillary: seen with neutrophilic infiltrate (bacterial etiology)

51
Q

Kaposi sarcoma Tx

A

Start anti-retroviral therapy in patient who is HIV(+) and hasn’t started it yet.

Lesions should shrink in response to therapy

52
Q

What viruses are in the polyomavirus family?

A

JC Virus

BK Virus

53
Q

What do polyomaviruses look like?

A

circular double stranded DNA - it’s a circular virus

54
Q

JC Virus

A

A polyomavirus

John Cunningham Virus

Causes progressive multifocal leukoencephalopathy (PML)

Greater than 50% of population has JC Virus, but it doesn’t cause problems if immune system is intact.

When it is immunocompromised (HIV with CD4

55
Q

How do you differentiate JC Virus from Toxoplasmosis?

A

Toxo: Brain lesions are ring-enhancing
JC: Non-enhancing lesions

56
Q

BK Virus

A

Type of polyomavirus

Famous for causing nephropathy and other urinary tract problems like hemorrhagic cystitis

Usually kidney and bone marrow transplant patients at risk

57
Q

Provide presentations for JC and BK virus infection

A

Polyomaviruses

1) JC with PML

40 yo HIV positive patient is complaining of weakness, visual changes, and difficulty with speech which has been getting worse over the last few weeks. CD4 = 158. CT/MRI shows multiple non-enhancing brain lesions.

2) BK

50 yo renal transplant patient taking immunosuppressants who presents with fever and gross hematuria

58
Q

What is the most common STD?

A

HPV - nearly all sexually active people will get HPV at some point.

59
Q

HPV 1-4

A

Verruca vulgaris = cutaneous common wart

Children get it on hands/feet

Transmission requires physical contact

60
Q

HPV 6, 11

A
  • Laryngeal papillomatosis = Recurrent respiratory papillomatosis

Tumors (papillomas) develop in airway

Typically in children

6 and 11 are typically contracted by kids during vaginal birth

  • Anogenital warts = condyloma acuminata

Seen in sexually active individuals

Acquired through sexual contact

61
Q

HPV 16, 18

A

Anogenital cancers - squamous cell carcinomas (cervical, vulvar, vaginal, penile, anal) - HPV infects squamous cells.

16 and 18 together cause 70% of cervical cancers

HPV 31, 33 also associated with these cancers.

Spreads through sexual contact. Condoms/Abstinence can prevent infection

62
Q

HPV Vaccine

A

Covers 6, 11, 16, 18 (NOT 31, 33)

16 and 18 cause 70% of cervical cancers

Guardasil - inactivated subunit vaccine

Recommended for women and men age 9-26 regardless of sexual activity.

63
Q

HPV cancer mechanism

A

HPV is able to disrupt regulation of the cell cycle

Tumor suppressors p53 and RB inhibit transition from G1 to S phase. (RB = retinoblastoma protein)

HPV encodes 2 proteins E6 and E7 that promote proteolysis of p53 and RB respectively

HPV takes out tumor suppressors therefore increasing risk of cancer.

Uninhibited cell growth leads to neoplasia

Cervical cancer buzzword: Patient who complains of post-coital bleeding

64
Q

Cervical cancer screening

A

Pap Smear lowers incidence of cervical cancer through early detection

Samples cervical cells from area called the transformation zone. This is where squamous epithelium from outer cervix (ectocervix) comes in contact with columnar epithelium from inner portion (endocervix)

Infected cells have morphological changes - Koilocytes (look like blue sunny-side eggs) - large, dense, wrinkled nucleus/maybe binucleate

65
Q

Risk factors for developing cervical cancer

A

Immunosuppression

HIV(+)*** (may enhance E6 and E7 expression AND immunocompromised)

Cervical/anal/penile cancers are AIDS-defining illnesses

66
Q

What disease is linked to Parvovirus B19?

A

Fifth Disease - “Slapped Cheek Fever”- Erythema Infectiosum

67
Q

Fifth Disease presentation in children

A

Low grade fever for 1 week

Fever breaks and kid develops slapped cheek rash on face

Then progresses to lacy, reticular pattern that travels down the body

68
Q

Parvovirus B19 infection presentation in adults

A

Usually schoolteachers

Joint pain, arthritis, edema

In patients with Sickle Cell Disease:

Aplastic anemia - caused by depletion of the bone marrow. When all cell lines are depleted the bone marrow is left with only adipocytes. When packed together they look like “cobwebs” - This is a transient effect and should fade as virus is cleared

69
Q

Parvovirus B19 genetics

A

It is the only single stranded DNA virus

Smallest DNA virus

70
Q

Parvovirus B19 transmission

A

respiratory droplets

Vertical (TORCH)

71
Q

Congenital Parvovirus B19 infection

A

Baby in-utero exposed to parvovirus

Exposure in Trimesters 1-2: Hydrops fetalis (severe fatal anemia that leads to fetal version of CHF)

Same thing happens in alpha-thalessemia

72
Q

What is the most common cause of tonsilitis and adenoiditis?

A

Adenovirus

73
Q

Adenovirus transmission

A

Respiratory droplets

Fecal-oral

74
Q

Adenovirus vaccine

A

Live attenuated

ONLY for military recruits

75
Q

Adenovirus presentation

A

Common in little children, military recruits, and those who frequent public pools - outbreaks in military barracks and public pool swimmers

Causes hemorrhagic cystitis - bladder infection leading to gross hematuria

Also a cause of viral conjunctivitis (pink eye)

76
Q

Hepatitis B replication

A

Inside AND outside of nucleus

77
Q

Hepatitis B genome

A

It is circular and partially double-stranded - It becomes fully double stranded during replication.

Goes from partially dsDNA –> ssRNA intermediate –> dsDNA

Carries a reverse transcriptase

Does not integrate into host chromosome so it is NOT a retrovirus like HIV

78
Q

Hepatitis B transmission

A

Sex, sharing blood products, sharing drug needles, vertical (TORCH)

79
Q

Vertical transmission of Hepatitis B

A

Low transmission.

Happens during delivery, not across placenta (the virus is too big)

Requires mixing of blood during delivery

80
Q

hepatitis B presentation

A

1) Hepatitis:

RUQ pain, jaundice

Some acute and some chronic (less likely than in Hep C tho - 5-10% of patients)

Younger kids are more likely to develop chronic infection - newborns infected have a 90-95% chance of becoming chronic

2) Extra-hepatic manifestations of Hep B
1) Prodromal serum sickness type illness with rash and arthralgias - purpural rash with non-blanching dark macules
2) Polyarteritis nodosa - systemic vasculitis that affects medium to small arteries, small aneurysms forming in the arteries have a “beads on a string” appearance.

Polyarteritis nodosa causes kidney damage (low GFR, HTN) by affecting vessels leading to the kidney

3) Membranous glomerular nephritis
4) Membranoproliferative glomerular nephritis

81
Q

Liver enzymes in Hepatitis

A

Viral hepatitis causes higher liver enzymes - ALT > AST

Hepatitis from alcohol raises enzymes too - AST > ALT

ALT is normal early on in neonatal hepatitis

82
Q

HBsAg

A

Hep B surface antigen

Marker for active disease

First to be clinically measurable

(+) = active infection - acute or chronic

Pt has symptoms

83
Q

HBeAg

A

Hep B Antigen that appears after HBsAg

Correlates with infectivity

(+) = infective

Pt has symptoms

84
Q

Anti-HBc

A

Core antibody for Hep B

(+) during window period

First antibody detected

85
Q

Anti-HBe

A

Antibody to E antigen in HepB

If this is presence there is low infectivity

86
Q

Anti-HBs

A

HepB

Indicates recovery

Pt no longer has infection (acute OR chronic)

This is always the value to check for immunity

87
Q

Order of appearance of Hep B serologies

A 
HBsAg
HBeAg
Anti-HBc
Anti-HBe
Anti-HBs
88
Q

Hepatitis B immunization in serology

A

Immunized person would be (+) for Anti-HBs - This is the only thing you’d see for vaccination.

If you also see Anti-HBc or Anti-HBe this would indicate that the person was infected at one point in the past.

89
Q

Chronic Hepatitis B

A

Long-term sequelae:

1) Cirrhosis
2) Hepatocellular carcinoma (higher risk)

90
Q

Hepatitis D

A

Cannot cause infection without Hep B

Hep D is an RNA virus that is:

1) enveloped
2) RNA (-) Sense
3) Circular RNA genome

Requires HBsAg to be infectious

2 types of Hep D:

1) Co-infection - when both viruses are transmitted simultaneously
2) Superinfection - when Hep D is transmitted on top of existing Hep B infection - worse outcomes

91
Q

Hep B Tx

A

Acute - will most likely clear up on its own.

Pregnant women and people who have progressed to chronic should seek Tx

Tx will not eradicate - it minimizes damage by preventing replication

Antivirals like Lamivudine and other NRTIs

Also interferon alpha

Give at risk kids anti-HepB immunoglobulins (IgG)
- If mom is Hep B (+) you must give immunoglobulins and Hep B vaccine to newborn for both active and passive immunity

92
Q

Pox virus replication

A

It is the only DNA virus that completely replicates in the cytoplasm

It comes with everything it needs inside it already - makes its own envelopes (doesn’t take it from host)

It packs its own RNA Polymerase that reads DNA - so it can just make mRNA right in the cytoplasm and get it processed by local ribosomes into proteins.

It makes all the proteins it needs, even its own DNA Polymerase

93
Q

What does Pox virus look like on biopsy?

A

Pox forms Type B inclusions (Guarnierni Bodies) - sites of viral replication in cytoplasm

Intracytoplasmic is diagnostic for Pox

94
Q

What viruses belong to the pox family?

A

Cowpox

Smallpox

Molluscum Contagiosum

95
Q

Cowpox

A

A type of Pox virus

Transmitted via contact with infected cow utters

The source of smallpox vaccine

96
Q

Smallpox

A

Vareola - a type of pox virus

Only exists in labs that study it - can be a bio weapon

Causes raised blisters on skin and mucosal surfaces

Lesions are all the same age/stage of healing

97
Q

Molluscum Contagiosum

A

Type of pox virus

Flesh-colored, dome-shaped, umbilicated (has little dimple in the middle) skin lesions - looks like snail shell

Mostly seen in children

Can be anywhere but palms/soles - mainly seen in trunk, axilla, antecubital fossa, popliteal fossa

In adults, it’s related to sexual transmission - single, umbilicated lesion - if it spreads diffusely person probably has HIV and is immunocompromised.

98
Q

What does Pox virus look like?

A

It is the largest DNA virus!

Its core is dumbbell shaped

Viruses (3 decks)

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