Viral Path, Lab, Herpes Lect 34, 35 Micro Exam 3

Front 1

What are the 3 main types of virus infection of a cell?

Back 1

1. abortive infection - failed infection. no viral replication, may be due defective virus or non permissive cell.
2. lytic infection- results in cell death
3. persistent infection - infection w/o cell death

Front 2

What does lytic infection result in? What does it occur?

Back 2

a. often due to viral inhibition of host cell DNA, RNA, protein synthesis.

b. replication of virus and accumulation of viral proteins can disrupt structure/functions
of cell. Inclusion bodies (viral "factories") often formed in nucleus or cytoplasm.

c. expression of viral proteins on cell surface can elicit immune-mediated cytolysis.

d. induction of apoptosis.

e. expression of viral proteins on cell surface can induce cell fusion and the formation
of syncytia (multinucleated giant cells); mechanism of spread.

f. These effects (and others) of virus infection on cells are called cytopathic effects
(CPE); can be used diagnostically.

Front 3

Name and describe 3 categories of persistent infection

Back 3

a. Chronic: productive, non-lytic; virus released by budding.
b. Latent: limited/no viral gene expression, no production of virus, but virus production
can often be re-activated.
c. Transforming: immortalization of cell by oncogenic viruses

Front 4

How do viruses enter into the body?

Back 4

a. Skin via abrasions, direct inoculation, arthropod vectors, animal bites.

b. Mucosal surfaces of the respiratory tract. Despite many protective mechanisms,
this is a major site of viral entry!

i. Mucous and ciliated epithelial cells in nasal cavity and most of lower respiratory
tract help clear foreign material to pharnyx, then it is coughed out or swallowed.

ii. Humoral (IgA, IgE) and cellular (local macrophages) protective mechanisms.

iii. Cool temperature of the upper respiratory tract inhibits replication of many
viruses.

iv. Some viruses remain local; others become systemic.

c. Mucosal surfaces of the gastrointestinal tract (fecal-oral route)-another major
site of viral entry!
i. Viruses entering the host via ingestion and carriage to the intestinal tract may
initiate local or systemic infections. Systemic infection occurs when virus crosses
the mucosal layer to invade underlying tissues and spreads within the host.

ii. Environment in the upper GI tract is harsh: intraluminal pH is ~2

Front 5

What is primary replication?

Back 5

a. Viral replication usually occurs at the site of entry, in permissive cells.

b. Viruses that replicate and remain at the site of entry produce localized infections

Front 6

What is a incubation period?

Back 6

a. The time interval between infection of the host and the onset of clinical symptoms.
During the incubation period, virus is amplified and may spread to a secondary site
to produce a disseminated or systemic infection.

b. Symptoms are caused by virus-induced tissue damage due to cytolytic effects or
immunopathogenesis. May be preceded by the prodrome (nonspecific, early, flu-
like symptoms.

Front 7

How do viruses spread from site of entry to target tissues?

Back 7

i. Local spread on epithelial surfaces.

ii. Subepithelial invasion and lymphatic spread
a. Viruses that penetrate the epithelium and basement membrane are exposed
to tissue macrophages and can enter the lymphatic system. Viruses are then
carried to local lymph nodes where they are exposed to macrophages-some
are engulfed, inactivated and processed for presentation, but some viruses
can replicate in macrophages, or can infect lymphocytes and thereby enter
the bloodstream.

iii. Spread by the bloodstream
a. The presence and transport of virus in the blood is called viremia.
i. primary viremia-due to virus replication at the primary site of entry.

ii. secondary viremia-due to virus replication at a secondary site, that may or
may not be the target tissue. Ex. macrophages, endothelial cells

b. Virus may be free or cell-associated.

c. Viremia is the most effective means of virus spread to all parts of the body.

iv. Peripheral nerves
a. Rabies virus, varicella zoster virus and herpes simplex virus

Front 8

How do viruses invade target tissue?

Back 8

i. Invasion of skin via the bloodstream-usually produces generalized rash. Lesions
described as macules, papules, vesicles, pustules, nodules.

ii. Invasion of the CNS:
a. via the bloodstream (hematogenous).
b. via infected meninges or cerebral spinal fluid (CSF).
c. via peripheral and sensory (olfactory) neurons.

iii. Invasion of other organs
a. Any other organ can be infected by viruses disseminated via the bloodstream.
Ex. Liver (Ex. HBV, HCV, HDV)
Ex. Testes, salivary glands, mammary glands, kidney tubules, and lungs may
lead to excretion of virus in semen, saliva, breast milk, urine, respiratory
secretions.
Ex. Fetus-some viruses may cross the placenta and either infect the placenta
or the fetus leading to abortion, fetal death, or teratogenic effects (Ex.
rubella virus, CMV).

Front 9

What determines viral cell and tissue tropism?

Back 9

i. Viruses require the presence of specific receptors, transcription factors, proteolytic
enzymes, and other factors for replication and pathogenesis. If these factors are
not present, virus cannot replicate. The requirements are different for each virus
and limit the cell types in which virus can replicate.

Front 10

How do viruses produce disease?

Back 10

i. Kill the cells they infect.

ii. Impair specialized functions of the cells they infect.
Ex. hormone production by a glandular cell
Ex. immunosuppression

iii. Elicit immune responses: Immunopathogenesis
a. Innate response (interferon, lymphokines) produces prodrome.

b. Adaptive response may exacerbate viral disease, especially with enveloped
viruses.
i. Cell-mediated immune response, CTL's.

ii. Immune complex deposition.

iii. Autoimmunity-viral antigens may "mimic" host antigens and elicit cross-
reactive immune responses.

Front 11

Nme the factors that affect susceptibility to and severity of viral disease

Back 11

i. Virulence refers to the ability of a virus to cause illness or death in an infected
host relative to other strains of the same agent. Virulence is not an absolute
property of a virus strain-it depends on both host and viral factors:
a. nature of the exposure (route of infection).
b. immune status, age, and general health.
c. viral dose.
d. genetics of the virus and the host.
e. ability of the host to repair damage.

Front 12

Descrube te recovery or convalscence of viral infection?

Back 12

a. Acute vs. chronic infections.

b. Symptoms of the viral infection may continue through the recovery period as tissue
damage is repaired.

c. In most (but not all) cases, the host develops resistance to challenge with the same
or similar strains of virus via a memory immune response.

Front 13

What are the 3 principles that all viral diagnostic techniques are based on?

Back 13

1. Viruses are intracellular parasites whose mission is to generate progeny viruses.
2. Viruses are composed of 2 distinct components: nucleic acid and protein.
3. Viral infections elicit virus-specific immune responses.

Front 14

What does the proper interpretation of a specimen depend?

Back 14

1. Timing: collect specimen(s) immediately after disease onset.

2. Selection: type of specimen collected depends on type of clinical disease & suspected
pathogen.

3. Transport: collect specimen into transport media which stabilizes viral infectivity.

4. Processing: as soon as possible, or hold at 40C.

Front 15

Describe the cell culture technique. What are the disadvantages?

Back 15

a. “Gold standard”, simple, sensitive, “open-minded”, allows amplification of virus for
additional assays.

b. Disadvantages: not all viruses grow in cell culture, not all viruses grow in all cell
lines-have to pick the appropriate cell line for suspected virus, can take a long time
for virus to grow.

Front 16

Presumptive diagnosis of viruses in culture..
1. Cytopathic effect?
2. Hemadsorption?

Back 16

i. Cytopathic effect (CPE): pattern, rate of formation, cell lines affected.
Ex. syncytia formation, deformed cells, viral inclusions, dead cells or plaques.

ii. Hemadsorption: attachment of red blood cells to surface of virus-infected cells.

Front 17

What are the advantages and disadvantages of direct detection methods?

Back 17

Advantages: fast, does not require infectious virus.
Disadvantages: amount of virus is limited, less sensitive than culture methods; for
immunostaining assays, have to choose specific antibodies.

Often used after amplification of virus in culture.

Front 18

Light microscopy

Back 18

Light microscopy of histologically stained clinical material-look for syncytia,
deformed cells, viral inclusions, etc. Most rapid method, but sensitivity and specificity
varies.
Ex. Tzanck smear for herpesviruses
Ex. Papanicolou smear for HPV

Front 19

Electron microscopy

Back 19

a. Advantages: for viruses that cannot be cultivated in normal cell cultures.

b. Disadvantages: expensive, requires expertise, need high concentration of virus.

Front 20

Immunostaining for viral proteins

Back 20

a. Use of virus-specific antibody (monoclonal or polyclonal) to detect viral antigens in
specimen. Have to pick the right antibody!
Ex. ELISA (enzyme-linked immunosorbant assay), agglutination assays

Ex. Detection of respiratory viruses in nasopharyngeal aspirate. Cells are placed in
multiple wells of microscope slide and tested with panel of virus-specific
antibodies.

Front 21

Describe PCR

Back 21

i. Amplifies DNA, or cDNA generated from viral RNA (reverse transcriptase, RT-
PCR), by using oligonucleotide primer sets complementary to virus target
sequences 50 to 1500 nucleotides apart on opposite strands of the DNA.

ii. VERY sensitive-may detect viruses which have nothing to do with disease, or
viral nucleic acid from contamination (big problem).

iii. Proper processing of specimens is critical to minimize degradation of nucleic
acid.

iv. Have to pick the right primers!

Front 22

Serodiagnosis
1. What are most diagnostic methods based on?
2. What does detection of virus specific igG antibodies indicate?
3. How about detection of igM antibodies?

Back 22

1. Most diagnostic methods are based on the demonstration of a significant rise (at
least 4-fold) in antibody titers between an acute serum, taken at or very near the
time of onset of symptoms, and a convalescent serum obtained at 10 to 14 days
later ("paired sera").

2. Detection of virus-specific IgG antibodies in serum indicates prior infection and
seroconversion.

3. Detection of virus-specific IgM antibodies in serum indicates current or recent
infection (within days to 1-2 months of infection).

Front 23

Serodiagnosis
1. What causes an anamnestic response?
2. What does serology provide an alternative to?

Back 23

4. Re-infection or recurrence later in life causes an anamnestic (secondary or booster)
response, in which a rapid (~3 days) and significant rise in virus-specific antibody
concentration occurs.

5. Serology provides an alternative method when sampling or transport conditions for
virus culture cannot be met, for viruses that are difficult to culture, when molecular
testing is not feasible, or in viral infections in which virus shedding has ceased when symptoms are detected.

Front 24

1. What technique specifically can be used to detect viral antibodies?

Back 24

Ex. ELISA, agglutination assays

Ex. Immunoblot (Western) Technique
Viral proteins are denatured and separated by gel electrophoresis, then transferred to a membrane. The membrane is incubated with the patient’s serum to allow antibodies to bind to immobilized viral antigens. Labeled secondary antibody is used to detect bound patient antibodies.

Front 25

Other methods of viral antibody detection:
1. neutralization of infectivity
2. hemagglutination inhibition

Back 25

a. Neutralization of infectivity: failure of a standard virus to grow in cell culture
after incubation with serum specimen dilutions.

b. Hemagglutination inhibition: failure of antibody-bound virus to
hemagglutinate red blood cells.

Front 26

What can happen at any time to latent herpesvirus infections?

Back 26

can be reactivated when the host’s cell-mediated immune response becomes suppressed during periods of normal stress, pregnancy, exposure to sunlight, or in more serious situations like HIV infection or cancer treatments. Reactivation may result in clinical symptoms that are similar (generally less severe) to those seen during a primary infection or they can be very different. In immunocompent people, reactivated disease generally resolves, but can recur

Front 27

Structure of herpesvirus
1. What is it enveloped with?
2. What's a tegument?
3. Describe its genetic code

Back 27

1. enveloped with icosahedral capsid
2. has tegument: viral proteins and enzymes involved in replication initiation
3. Virus encodes its own DNA polymerase, which is the target of antiviral drugs.

4. Sensitive to inactivation by desiccation, detergents, low pH.

5. Double-stranded DNA genome, relatively large, encodes ~70-100 proteins.

Front 28

Describe the steps of replication for herpesvirus

Back 28

1. Virus binds cellular receptor and enters by fusion of envelope with cell membrane.

2. Nucleocapsid and viral proteins in tegument are released into cytoplasm.

3. Nucleocapsid docks at nuclear membrane and genome enters nucleus.

4. Genome is transcribed by the host DNA-dependent RNA polymerase and replicated (by the
viral DNA polymerase) in the cell nucleus; a highly coordinated process.
a. Different genes are expressed in lytic vs. latent infections.
i. Genome is not replicated in latent infections.

b. Immediate early (IE) gene expression produces viral proteins involved in viral gene
transcription.

c. Early gene expression produces more transcription factors and enzymes, e.g. viral
DNA polymerase, thymidine kinase.

d. Viral genome is replicated by the viral DNA polymerase—a good target for antiviral
drugs.

e. Late (after genome replication) gene expression produces mainly structural proteins.

5. Viral proteins are synthesized in the cytoplasm and transported to the nucleus wher

Front 29

Epidemiology of herpes simplex virus types 1 and 2 (HSV-1, HSV-2)

Back 29

1. HSV-1: most often through saliva
HSV-2: through sex
2. 80% have HSV-1 and experience reactivation (cold sores)

c. Most people are exposed to HSV-1 as children; most people are exposed to
HSV-2 when they become sexually active.
d. HSV-1 is usually found in oral infections and HSV-2 is usually found in genital
infections, but both viruses can cause infections in both places, if introduced.
e. The number of HSV-2 infections is increasing; HSV-1 infections are stable.
f. HSV-1 and HSV-2 can be transmitted during symptomatic and asymptomatic
shedding of the virus.

Front 30

Pathogenesis and immunity for HSV-1 and HSV-2
1. Where's the pirmary replication site?
2. How do the cells spread infection?
3. Describe the immune system response

Back 30

a. Primary replication site: initial site of infection in skin or mucous membrane.
b. Virus forms syncytia and can spread cell-to-cell. Vesicles containing virions and
cell debris are formed. Vesicles are clear with an erythematous base.
c. Virus enters neurons and migrates to the sensory ganglion cells where it
becomes latent (no virus production).
i. HSV-1 in trigeminal ganglia
ii. HSV-2 in lumbar and sacral ganglia
d. Immunity is type-specific, with some cross-protection, but it is incomplete;
re-infection and reactivation can occur. Cell-mediated immunity and antibodies
are important in suppressing severe disease.

Front 31

Clinical manifestations
1. HSV-1 and HSV-2
2. What would reactivation symptoms look like in each?
3. What is a major disease associated with HSV?

Back 31

a. Primary infections may be symptomatic or asymptomatic in immunocompetent
hosts:
i. HSV-1: gingivostomatitis: lesions in mouth, on tongue; herpetic whitlow
on finger
ii. HSV-2: genital lesions (painful, may itch)
iii. Lesions last 1-2 weeks, then heal

b. Reactivation of viral replication can occur later, usually when cell-mediated
response is reduced by stress, sunlight, hormonal changes, or fever, resulting in
“cold sores” (HSV-1) or genital herpes (HSV-2) at the original site of infection.
Recurrent episodes are usually less severe and shorter than primary infection;
they generally resolve, but can recur.

c. Primary and recurrent infections in immunocompromised patients and neonates
are always more severe and may become disseminated.

d. Ocular disease
i. HSV is an important cause of conjunctivitis and can lead to keratitis;
HSV is the most common cause of viral keratitis, which can be severe.
It is more common in adults and likely due to viral reactivation; HSV
conjunctivitis is more co

Front 32

Descirbe the lab diagnosis of HSV-1 and HSV-2.

Back 32

a. Tzanck smear for presumptive diagnosis.
b. Detection of viral antigens in skin scrapings, or specimen which has been
inoculated into cell culture.
c. PCR
d. Rise in antibody titer (only for primary infection).

Front 33

Treatment for HSV-1 and HSV-2

Back 33

a. None necessary for mild disease in immunocompetent hosts.
b. Acyclovir can used to treat serious primary and recurrent infections; limits
duration and severity of symptoms; no effect on latent virus!
c. Valacyclovir (Valtrex) and famciclovir (Famvir) are used to treat genital herpes
and to suppress recurrences.
d. Acyclovir is the prototype anti-HSV drug and its mechanism of action involves
binding to the viral DNA polymerase and preventing viral DNA replication. It is
activated only in HSV-infected cells by the viral thymidine kinase (and cellular
enzymes).
e. Acyclovir and its derivatives are called nucleoside analogues.

Front 34

Prevention of HSV-1 and HSV-2?

Back 34

a. Avoid contact with obvious lesions.
b. Healthcare workers need to wear gloves when touching patients.
c. No sexual contacts during outbreaks; condoms; counseling.
d. Counseling for HSV-infected pregnant women: Caesarian delivery
e. Prophylaxis to prevent recurrences.
f. Hand washing with soap and water can inactivate the virus!
g. Remember—asymptomatic shedding of the virus occurs

Front 35

Varicella Zoster epidemiology
1. Where does it occur?
2. How is it transmitted?
3. What population is primarily infected?

Back 35

a. Virus occurs worldwide; no seasonal variation in incidence.
b. VZV is very contagious before and during symptoms.
c. Transmitted by respiratory route or contact with skin vesicles.
d. Who gets infected and sick?
i. Children, ages 5-9 y.o. get mild, “textbook” chickenpox.
ii. Teens and adults at risk for more severe form of chickenpox and
pneumonia.
iii. Immunocompromised and newborns at risk for life-threatening
complications of chickenpox, including pneumonia, encephalitis,
progressive disseminated varicella.
iv. Elderly and immunocompromised, who have been previously
infected, are at risk for recurrent disease:
a. Herpes zoster (shingles)
b. Postherpetic neuralgia

Front 36

Pathogenesis and immunity of Varicella Zoster
1. Where's the primary replication site?
2. How does the virus spread, adn wat does it produce in response?
3. How does the immune system react?

Back 36

a. Primary replication site: upper respiratory tract mucosa.
b. Virus spreads via lymphatics and bloodstream (primary viremia) and targets
reticuloendothelial cells. Virus forms syncytia and can spread cell-to-cell.
c. Secondary viremia results in spread of virus throughout body to the skin.
i. Vesicular rash appears in successive crops.
ii. Fever and systemic symptoms occur at same time as rash.
d. Virus then becomes latent in dorsal root ganglia-no virus is produced.
i. Reactivation of viral replication can occur later, usually when cell-
mediated immunity is reduced by aging, stress, or immunosuppression
due to other causes, resulting in “shingles” or postherpetic neuralgia.
e. Virus is produced, travels along neural pathway to skin producing rash along
dermatome of original infection; can be very painful and last for weeks (shingles)
or months (post-herpetic neuralgia).
f. Humoral response can limit viremia, but cell-mediated immune response is
important for resolving chickenpox.
g. Lifelo

Front 37

Clinical manifestations of varicella zoster

Back 37

a. Incubation period: 14-21 days.
b. Prodromal symptoms, including fever and malaise may occur.
c. Rash appears in crops, centrally first on the trunk and head (including scalp),
then spreads to the extremities; can occur in mouth, conjunctiva and vagina.
i. Evolves from papules to vesicles and pustules, then crusts; can see all
stages of skin lesions at one time, in contrast to lesions of smallpox.
ii. Itching can be severe.
d. Reactivation disease: shingles or post-herpetic neuralgia.

e. Ocular disease
i. Infection of the cornea can occur during shingles; scarring can occur.
ii. Retinitis can occur in congenital infections and shingles; not common in
chickenpox.
iii. Posterior uveitis can occur in shingles.

Front 38

Lab diagnosis of varicella zoster

Back 38

a. Diagnosis typically made on clinical presentation.
b. Laboratory tests: Tzanck smear, detection of viral antigens, PCR, serology.

Front 39

Treatment for varicella zoster

Back 39

a. None necessary for mild disease in immunocompetent hosts.

b. Adults and immunocompromised patients with VZV or shingles can be treated
with acyclovir, famciclovir (Famvir), or valacyclovir (Valtrex), which limit the
duration and severity of symptoms.

c. Varicella zoster immune globulin (VZIG) can protect immunosuppressed patients
from severe disease, but not during active varicella or zoster disease.

Front 40

Prevention of varicella zoster?

Back 40

chickenpox and zoster.
i. Effective in preventing varicella, but cannot prevent zoster in previously
infected people.
ii. Should not be given to immunocompromised people or pregnant
women.
b. A live, attenuated VZV vaccine (Zostavax) was FDA-approved in 2006 to prevent
zoster (“shingles”).
i. Contains a higher dose of the attenuated virus in Varivax.
ii. “Boosts” immune response against VZV to help reduce chances of a
zoster outbreak and to lessen severity of outbreak if it occurs.
iii. Recommended for people > 60 years old at risk
iv. Should not be given to immunocompromised people

Front 41

Epidemiology of Epstein Barr virus

Back 41

a. Found worldwide; more than 90% of adults in the U.S. have been infected.

b. EBV is transmitted by saliva; “kissing disease”.

Front 42

Pathogenesis of Epstein Barr
1. Where does it replication?
2. Where does it spread?
3. How does the immune system react?

Back 42

a. Primary replication occurs in the oropharynx, enters bloodstream, infects and
remains latent in B lymphocytes.
b. Cytotoxic T cells are activated against EBV-infected B cells and appear as
“atypical lymphocytes” (Downey cells) in a blood smear.
c. EBV-specific and non-specific antibodies are produced:
i. Viral-specific IgM and IgG antibodies can be used to identify current
vs. past infection.
ii. Heterophile antibodies are also produced in response to EBV infections (and some other infections). These antibodies can be detected using special test and used to make a presumptive diagnosis of EBV infection (Monospot test used when mononucleosis is suspected).

Front 43

Clinical manifestations of Epstein barr virus

Back 43

a. EBV infections acquired before 2-3 years old are usually asymptomatic.
b. EBV infections acquired later in life are more often associated with infectious
mononucleosis.
i. Typical symptoms include: fever, sore throat, lymphadenopathy,
splenomegaly (rupture can occur during contact sports!); anorexia, lethargy, and hepatitis can also occur.
ii. Recovery generally occurs after 2-3 weeks.

c. EBV is also associated with 4 other relatively rare, but serious diseases:
i. Oral hairy leukoplakia: whitish oral lesions that occur in AIDS patients resulting from productive infection of epithelial cells (opportunistic infection). EBV found in all cases.
ii. Burkitt’s lymphoma: B-cell lymphoma of the jaw and face found primarily in children in certain regions of Africa. EBV associated with some cases.
iii. Nasopharyngeal carcinoma (NPC): epithelial cell tumor found primarily in Asian adult populations. EBV associated with some cases.
iv. Hodgkin lymphoma: a type of B cell lymphoma; pathogenesis is complex, but so

Front 44

Lab diagnosis, treatment, and prevention of Epstein barr virus

Back 44

Laboratory diagnosis
a. Blood smears for atypical lymphocytes and serological tests for heterophile and
EBV-specific antibodies.

5. Treatment
a. None necessary for mild disease in immunocompetent hosts.
b. Acyclovir is not very effective, but can be used in life-threatening cases.

6. Prevention
a. No vaccine

Front 45

Epidemiology of cytomegalovirus
1. Who gets it? How it is transmitted?

Back 45

a. Over 80% of adults have been infected.
b. Transmitted by a variety of modes:
i. to babies: transplacentally, in the birth canal, breast milk
ii. among young children: via saliva
iii. among adults: sexual contact (semen, cervical secretions)
iv. blood transfusions, organ transplants

Front 46

Pathogenesis and immunity of cytomegalovirus

Back 46

Pathogenesis & Immunity
a. CMV becomes latent in leukocytes and persists in kidney and cervical cells.

b. Cell-mediated immunity is most important in controlling infection, but humoral
immunity also involved.

Front 47

What are the clinical manifestations of cytomegalovirus

Back 47

a. Infection of children and adults usually asymptomatic, but it can cause
heterophile-negative mononucleosis.

b. Illness in immunocompromised people usually due to reactivation of latent
infection: pneumonia, hepatitis; in AIDS patients often see diarrhea, retinitis. Big
problem in organ transplant patients.
i. CMV retinitis in AIDS patients is characterized by vasculitis, hemorrhage, and
exudates leading to retinal necrosis.

c. CMV is the most prevalent cause of congenital disease due to viral infection. When a pregnant woman is seronegative for CMV, i.e. has never been infected, and becomes infected during her pregnancy, the fetus is at risk for infection and disease, i.e. cytomegalic inclusion disease. This disease can affect many organs and result in serious congenital defects (mental retardation, deafness, death).Transmission can be intrauterine, perinatal or postnatal. Intrauterine is less frequent than perinatal transmission, but is associated with the most serious disease in neonates. Primary CMV

Front 48

Lab diagnosis of cytomegalovirus

Back 48

a. Cytomegalic cell: enlarged, infected cell with “owl’s eye”-a basophilic nuclear
inclusion body; infected cells found in infected body tissues and urine.
b. Detection of viral antigens by immunostaining or ELISA; detection of viral nucleic
acids by hybridization or PCR.
c. Serodiagnosis; heterophile-negative antibodies.

Front 49

Describe the treatment and prevention of cytomegalovirus

Back 49

a. None necessary for mild disease in immunocompetent hosts.
b. Gancyclovir for serious disease.
c. CMV immune globulin is used to prevent disseminated infection in organ
transplant patients.

6. Prevention
a. No vaccine.
b. CMV-infected infants shedding virus in their urine should be isolated from other
infants.
c. Screen blood and organs for transplantation.

Front 50

Who does human herpesvirus-6 affect?
How isit transmitted, what's the clinical symptoms.

What immune response is necessary to resolve the illness?

Back 50

HHV-6 causes a common and benign childhood exanthem, roseola (exanthem subitum, 6th disease). The virus is transmitted by saliva and clinical symptoms include the rapid onset of a high fever that lasts a few days, followed by a generalized rash that last a day or two. Cell-mediated immune response is necessary to resolve the illness. Virus remains latent in T cells and monocytes.

Front 51

Kaposi's sarcoma associated herpesvirus

What is it the most common cause of in AIDS patients?

Back 51

KSHV is the most common cause of cancer, Kaposi’s sarcoma (KS), in AIDS patients. It is primarily an opportunistic infection occurring in AIDS patients, but the virus can be found in immunocompetent people with no evidence of disease. It is transmitted by sexual contact and organ transplants. KS is a malignancy of vascular endothelial cells resulting in dark purple lesions on the skin and internally.