HHV7 Flashcards
HHV7 structure and classification
Betaherpesvirus
Linear dsDNA
3 main structural elements shared by all herpes viruses:
- Nucleocapsid - icosahedral contains viral DNA genome
- Envelope with embedded viral glycoproteins
- Tegument - protein mixture occupying space between nucleocapsid and envelope
Baltimore: I
HHV7 tropism & viral entry
lymphotropic virus that replicates in CD4 T lymphocytes. It can be induced from latency within T cells by cell activation
HHV-7, unlike HHV-6, utilizes CD4 as a cellular receptor for entry into cells. Thus, HHV-7 infection interferes with HIV-1 infection. HHV-7 does not require CXCR4 for entry but may downregulate its expression with potential implications for HIV-1 coinfection.
HHV7 epidemiology
HHV-7 is ubiquitous. More than 95 percent of adults are seropositive. Infection with HHV-7 generally occurs during childhood but peaks at a later age than infection with HHV-6, usually around 3 years of age.
Shed in saliva and other bodily fluids.
HHV7 clinical manifestations
- Generally asymptomatic.
- Primary infection: fever & rash, febrile seizures, exanthem subitum & roseola infantum, hepatitis, IMN.
Rare: encephalitis, meningitis, lichen planus.
HSCT transplant: HHV-7 DNA in peripheral blood lymphocytes was associated with a longer time to neutrophil engraftment and with symptomatic CMV disease.
HHV7 diagnostics & treatment
PCR
Serology - reasearch assays
In vitro, foscarnet and cidofovir inhibit HHV-7 replication by achievable concentrations. The virus is relatively resistant to acyclovir, penciclovir, and ganciclovir.
Small clinical studies suggest that HHV-7 is resistant to ganciclovir at levels that were effective for prevention and treatment of CMV. Sensitivity of HHV-7 to the guanine analogs was different from HHV6, suggesting a difference in selectivity of specific viral enzymes.