Viruses Flashcards

1
Q

Herpes simplex virus

A

HSV-1 and HSV-2; infect and replicate in mucoepithelial cells; produce latent infection in nerve ganglia; reactivation can be induced by sun exposure, fever, trauma, stress

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2
Q

What are the manifestations of Herpes simplex virus and how is it treated?

A

HSV-1: (above the waist, oral herpes) grouped or singular vesicular lesions that become pustular and then ulcerate (core sore/fever blister); primary and recurrent activation can be asymptomatic; infection of the eye can cause blindness, encephalitis
HSV-2: (below the waist, genital herpes) 15-30% of sexually active adults are positive for it; multiple painful vesiculopustular lesions that eventually ulcerate; can be transmitted to neonates at birth (60% mortality rate; high chance of neurological issues)
Treatment: acyclovir and other antivirals

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3
Q

Human Herpesvirus 6

A

causes roseola (typically in children); usually only a major concern for immunocompromised patients

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4
Q

What are the manifestations of Human Herpesvirus 6 and how is it treated?

A

roseola- high fever, body rash; self-limiting in 1-2 days; rare complications include encephalitis, bone marrow diseases, and other CNS problems
Treatment: experimental, cidofovir and ganciclovir have been shown to be effective

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5
Q

Varicella- zoster virus

A

acquired via respiratory route, usually before adulthood; causes chickenpox then shingles due to reactivation later in life; replicates in the upper respiratory tract, then spreads via viremia; infects skin and causes an immune response (chickenpox lesions); latently infects sensory ganglion cells

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6
Q

What are the manifestations of Varicella- zoster virus and how is it treated?

A

varicella (chickenpox) widespread vesicular, itchy rash; can cause severe disease in immunocompromised patients; self-limiting; herpes zoster (shingles) reactivation of the varicella-zoster virus, very painful rash, postherpetic neuralgia can occur
Treatment: acyclovir and other antivirals can be used; live vaccine available

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7
Q

Hepatitis B

A

hepadnaviridae family; 240 million people are chronically infected; more than 680,000 die every year due to complications (cirrhosis, cancer); 50% of HBV infections in the US are sexually transmitted; needlestick transmission is a risk for healthcare workers; vertical transmission can occur during the birthing process; chronicity extremely high in vertically infected infants; strong association between HBV chronic infection and hepatocellular carcinoma (HCC)

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8
Q

What are the manifestations of Hepatitis B and how is it treated?

A

clinical picture is highly variable, incubation period of 30-180 days; acute hepatitis B usually involves the gradual onset of fatigue, loss of appetite, nausea, pain, and fullness in the right upper abdominal quadrant; arthritis and rash can occur early on; increasing cholestasis and hence clay colored stools, darkening of the urine, and jaundice; symptoms may persist for several months before resolving
Treatment: no specific treatment for acute infection; interferon and reverse transcriptase inhibitors are used in chronic infection; no cure

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9
Q

Human immunodeficiency virus (HIV)

A

A retrovirus that specifically targets the CD4+ T cells of the immune system
- transmission of HIV (sex), acute phase of intense viral replication and spread to lymphoid tissue; flu or mono-like illness; activation of innate and adaptive immune response but unable to contain the highly replicating and mutating virus; chronic asymptomatic phase (clinical latency) of continued viral replication; advanced phase of marked depletion of CD4 T-cells leading to development of AIDS
- AIDS, 1981 large number of rare skin cancers and opportunistic infections among homosexual males; transmission via anal and vaginal sex, intravenous drug use, exposure to bodily fluids; highest risk in receptive anal sex; mother to child transmission can occur; risk reduced due to antiretroviral therapy (ART) 36 million people live with HIV worldwide; 1.2 million in the US

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10
Q

What are the manifestations of Human immunodeficiency virus (HIV) and how is it treated?

A

early symptoms are like the flu; HIV infection is lifelong; progression to AIDs is highly variable among individuals; if untreated, could be a few years or more than 10; ART can suppress viral load to undetectable level indefinitely; AIDs leads patients to contract a wide spectrum of opportunistic infections
Treatment: 6 classes of antiretroviral agents; combinations of ARTs used in treatment to bring viral load down to undetectable levels within 6 months; HIV ART regimens recommended for post-exposure prophylaxis to prevent infection; ART recommended for all HIV infected individuals regardless of T cell count; viral load and T-cell count is monitored regularly to determine ART efficacy and immune deficiency

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11
Q

Influenza

A

respiratory virus. from the family orthomyxovirus (types A, B, C); influenza A is the most virulent and quickest to undergo genetic changes (antigenic shift); enveloped ssRNA virus
A: has 3 subtypes- H1, H2, H3 and 2 subtypes-N1 and N2 in humans
Human, animal, and avian strains are similar but may have differences in receptor specificities; direct droplet spread is the most common transmission; more common in winter months; cold may allow virus to survive longer in the environment
Virus multiplies in upper respiratory tract ciliated epithelial cells causing structural and functional abnormalities; there is an interference with the mechanical clearance mechanism of the respiratory tract; tissue damage creates susceptibility to bacterial invasion

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12
Q

Antigenetic drift in influenzae

A

In antigenic drift, a point mutation changes the antigenic structure of the hemagglutinin (H) and neuraminidase (N) proteins of influenza virus A, making an antibody developed against the original strain less effective at neutralizing the drifted strain.

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13
Q

What are the manifestations of Influenza and how is it treated?

A

short incubation period (2 days) followed by acute disease (fever, myalgia, headache, dry cough); improvement within a week, lingering problems for several weeks; can lead to pneumonia; bacterial superinfection if there is a sudden worsening of symptoms
Treatment: supportive therapy indicated; abx prophylaxis does not prevent bacterial superinfection; neuraminidase inhibitors are useful for types A and B; annual vaccine

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14
Q

Rhinovirus

A

picornavirus family; optimum growth temp is 33 degrees; common cold virus; more than 100 serotypes; mild URI lasting 3-7 days; minimal cell damage, self limiting

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15
Q

Rotavirus

A

most common cause of winter gastroenteritis in children less than 5 years; serious diarrheal disease in 3-35 months of age; destroys the villous cells of the jejunum and duodenum and produces a nonstructural protein that has enterotoxin-like effects (within the host cell)
- Rotavirus produces non-structural protein NSP4, which increases chloride permeability; increased chloride permeability increases fluid secretion in the gut and directly results in watery diarrhea and destruction of villous cells in the jejunum and duodenum.

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16
Q

What are the manifestations of Rotavirus and how it is treated?

A

abrupt onset of vomiting followed by watery brown stool; severe cases the stool can be clear; low grade fever; vomiting lasts 1-3 days and diarrhea lasts 4-8 days; severe dehydration can lead to death, small malnourished infants; increased chloride permeability leads to increased fluid secretion
Treatment: live oral rotavirus vaccines are recommended for infants

17
Q

Step # 1 in viral replication

A

Adsorption or attachment to host cell: attachment of viral surface proteins/spikes from the cell surface receptor proteins; capable of infection only a limited spectrum of cell types (host range) aka tissue tropism; most are limited to a single species they can infect; specificity is determined by the different cell receptors and virion attachment proteins (complementary surfaces)

18
Q

Step #2 in viral replication

A

Penetration/entry: enveloped viruses have 2 mechanisms (direct fusion which releases the nucleocapsid into the cytoplasm; and receptor-mediated endocytosis (viropexis) which forms an endosomal vesicle- acidified by the host cell) naked capsid viruses also enter cell by viropexis but do not have a membrane to fuse with the endosomal vesicle (lyse the vesicle)

19
Q

Step #3 in viral replication

A

Uncoating of the virus to release genome

20
Q

Step #4 in viral replication

A

Virion component production: most RNA viruses replicate in the cytoplasm, except influenza and retroviruses which replicate in nucleus; most DNA viruses replicate in the nucleus; transcription (virus-specific mRNAs that program the host cell ribosomes to synthesize viral proteins; host RNA polymerase; RNA- use genome as mRNA for early protein synthesis)
Genome replication
DNA viruses: smaller ones depend on host DNA replication machinery; larger viruses encode for enzymes necessary for DNA replication; can transform host cell into abnormal or cancerous cells (continual synthesis of viral proteins)
RNA viruses: must encode their own polymerases to replicate RNA

21
Q

Step #5 in viral replication

A

Assembly: encapsidation is the process of enclosing the viral genome in a protein capsid

22
Q

Step #6 in viral replication

A

Release of viral particles from the cell: cell death - die due to viral interference with normal cellular metabolic processes; leads to apoptosis; some naked capsid viruses are able to lyse the cell and are released; some are able to block/delay apoptosis to allow virus replication cycle to complete; budding where most enveloped viruses acquire an envelope during this process; membrane site first acquire virus-specific spikes

23
Q

Productive/Lytic infection

A

Active replication of virus; release of new progeny virus particles (often upon lysis of the host cell)

24
Q

Latent infection

A

nonproductive response; when the virus persists inside host cell, not replicating and host cell survives; can be associated with oncogenic transformation in some viruses; persistent infection

25
Q

Chronic infection

A

persistent infection; where a low level of virus is produced with little to no damage to target tissue

26
Q

Coxsackie A virus

A

single-stranded positive-sense RNA virus belonging to the Picornaviridae family. Coxsackievirus causes hand, foot, and mouth disease, characterized by vesicular lesions in the mouth and extremities

27
Q

Flaviviridae (Dengue virus)

A

causes characteristic skin lesions as well as fever and muscle and joint pain and is sometimes called breakbone fever

28
Q

Hepeviridae (HEV)

A

causes hepatitis transmitted by the fecal–oral route