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23 Cards in this Set

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Herpes simplex 2 --> General Notes
Glycoprotein-containing envelope, and therefore susceptible to drying, acid, solvents, and detergents. Space between capsid and envelope contain enzymes and viral proteins that initiate replication and this space is called a tegument. The envelope of Herpes comes from the nucleus of the Golgi membrane. Can be transmitted at time of birth
Herpes simplex 2 --> Area of body affected.
Type 2 - Usually genital, latent in sacral ganglia. Associated with cervical cancer.
Herpes simplex 2 --> Genome and replication
Double-stranded DNA envelope virus .LYSOGENIC...1-Latency (asymptomatic) is initiated by transcription by host polymerase in the cytoplasm (not integrated) . Infection initiated in mucous membrane, virus infects cells at site, and virus moves to innervating neurons, traveling to ganglion. Tissue damage is caused by virus infection and host response. Lesions heal with scarring. 2-Lytic cycle is when the genome has completed transcription performed by viral-encoded polymerase. 3-Regulated by viral-encoded and cellular nuclear factors 4-Scavenger enzymes provide DNA substrates to viral polymerase. 5-Recurrence activated by stress, virus travels down nerve and initiates another lesion at the same site. Recurrent infections are generally less severe, more localized, and heal more quickly.
Herpes simplex 2 --> epidemiology
Infected individuals remain infected (and infectious) for life. HSV is labile (enveloped). Transmitted sexually via vesicle fluid (kissing), saliva. 90% of third-wolrd invididuals have HSV 1 and antibody by age. If transmitted during birth, HSV 2 can cause disseminated and neurologic infection. Both types of herpes simplex cause the lesions in either the oral or genital regions, and can not be differentiated by look.
Herpes simplex 2 --> virulence factors
Infection initiated in mucous membrane (virus infects cells at site, and vius moves to innervating neurons, traveling to ganglion. Infection returns to the original site and produces vesicles (but may be inapparent). Herpes simplex has clever mechanisms to avoid antibody-mediated inactivation. Glycoprotein C (gC) binds and depletes complement. gE/gl complex binds Fc portion of antibody = camouflage. Infection is controlled by TH1-associated delayed-type hypersensitivity and cytotoxic killer T-cell (culprit = CD8). Humoral immunity (i.e. antibodies) is ineffective. Cell mediated immunity is responsible for many of the symptoms. In immunocompromised pateints HSV can disseminate to vital organs and brain. Tissue damage is caused by virus infection and host reponse and lesions heal without scaring. Encodes a protein which blocks TAP channel, thus can't get viral antigen thru TAP channel in order to be presented on MHC I which prevents recognition by CD8 cells.
Herpes simplex 2 --> Signs and symptoms of disease
Genital herpes - usually type 2, but can be type 1 (10%). Primary infection is asymptomatic (but maybe accompanied by fever, malaise, myalgia, inguinal adenitis indicating transent viremia); recurrences are painful; patients can usually predict recurrences (burning, itching); patients can be shedding virus even if asymptomatic.
Herpes simplex 2 --> Laboratory diagnostic
Serology is not useful because it is cell mediated. Tzanck Smear - scrape the base of a lesion, Pap stain shows giant cells and inclusions. Culture - sensitive and rapid (2-3 days), lab will usually tell you if it is type 1 or 2. Biopsy of brain - herpes can be seen by a good pathologist.
Herpes simplex 2 --> Treatment
The scavenger enzymes are targeted by some antiviral agents because they are different from host cell enzymes. Most drugs are nucleotide analogues and inhibitors of DNA polymerase. Acyclovir is activated by viral thymidine kinase (ON EXAM - acyclovir mechanism of action); incorporated by polymerase into viral DNA instead of tymidine; prevents elongation of DNA molecules; Resistance mechanism = inactivated viral thymidine kinase. Treatment may shorten symptoms but doesn't eliminate latent infection.
Varicella zoster --> General Notes
Child form: Extremely contageous- kids in daycare. 90+% of adults have serologic evidence of previous infection. The younger the child the milder the disease. Adult form: As older adults 10-20% of us will experience shingles. Adults with shingles may serve as a source of chickenpox in susceptible kids ("zoster form" = varicella).
Varicella zoster --> Epidemiology
Contract from infected individuals. Enters respiratory tract, then to the skin, and then spreads from skin to sensory neurons/dorsal root ganglia.
Varicella zoster --> Virulence Factors
Becomes latent in the dorsal root or cranial nerve ganglia. Controlled by CMI, and produces blisters. Spread by respiratory route
Varicella zoster --> Signs and symptoms of disease
Childhood primary varicell - incubation of 2 weeks. Initial site is the mucosa of the respiratory tract. Spread via circulatory system to cells of RES. Secondary viremia on day 10-13. Infects skin - itchy maculopapular/vesicular rash in successive crops with fever lasting 3-5 days. (more severe on trunk than on extremities, all stages observable at once, unlike smallpox, occur in mouth, vagina, and conjunctivae), vesicle becomes pustular and crust over, becomes latent in dorsal root or cranial nerve ganglia. Adult primary varicella - usually more severe than childhood disease. 20-30% get interstitial pneumonia, possibly fatal. Due to increased inflammatory response in adult. Reye's syndrome (encephlopathy and liver damage) due to increased inflammatory response in adult. Shingles (herpes zoster) - reactivation of infection. Rash follows a single dermatome. Very painful, 30% will have postherpetic neuralgia lasting years! Disseminated disease in immunocompromised hosts - potentially fatal
Varicella zoster --> Laboratory Diagnosis
You will not usually need to the lab to help make this diagnosis. Cytology of lesion base. Direct antigen test (FAMA = fluorescent antibody to membrane antigen), not widely available. Culture - just like herpes simplex and too expensive. PCR - expensive, but available. Serology - test for immunity (i.e. Serology = good).
Varicella zoster --> treatment
Treat with acyclovir, but it is less effective for VZV. Disease can be prevented with varicella-zoster immune globin (VZIG) - if child has been inoculated with it, then give immune globin against it to prevent outbreak. Vaccinate Chickenpox in kids doesn't need treatment unless immunocompromised
None
Varicella zoster --> Genome and Replication
Double-stranded DNA envelope virus. Incubation of 2 weeks. Initial site is the mucosa of the respiratory tract. Spread via circulatory system to cells of RES. Secondary viremia on day 10-13. Infects skin - itchy maculopapular/vesicular rash in successive crops with fever lasting 3-5 days. (more severe on trunk than on extremities, all stages observable at once, unlike smallpox, occur in mouth, vagina, and conjunctivae), vesicle becomes pustular and crust over, becomes latent in dorsal root or cranial nerve ganglia.
Parvovirus-->General Notes
Smallest ssDNA virus. Just one human pathogen - B19 attacks RBCs. Some Parvoviruses called Dependoviruses can only infect humans if they co-infect with an adenovirus, needed for replicative machinery. TRANSPLACENTAL
Parvovirus -->Area of Body Affected
RBC's
Parvovirus--> Genome and replication
Single-stranded DNA non-eveloped virus. Replicates in erythroid-progenitor cells, receptor is blood-group P anitgens
Parvovirus--> Epidemiology
Most common in young kids, 50% have antibody by age 15. Spread by droplet nuclei, later winter, spring.
Parvovirus--> Virulence Factors
Haemotopoeisis stops in four days, decline in hemoglobin. In adults, B19 causes acute, symmetric polyarthritis, often without rash (mediated by immune complexes). Severe effects in fetus, because RBC turnover is high and cell-mediated immunity is low.
Parvovirus--> Signs and Symptoms
Fifth Disease ON EXAM = Erythema infectiosum: aplastic crisis in patients with chronic hemolytic anemia, and acute polyarthritis in adults. "SLAPPED CHEEK SYNDROME" ON EXAM - distinctive rash that develops and spreads to arms and legs (subsides in 1-2 weeks). Fetus may develop myocarditis, severe anemia, secondary cardiac failure If fetus survives, no long-term sequelae ON EXAM. Some have fever, sore throat, malaise. Transient aplastic crisis in patients with chronic hemolytic anemia (sickle cell); dypsnia, lassitude, confusion
Parvovirus--> Laboratory diagnostics
Serology for Parviovirus B19 IgG and IgM; PCR for parvovirus DNA
Parvovirus-->Treatment
No Treatment