The Herpesviridae are a large family of DNA viruses that cause diseases in animals, including humans. The members of this family are also known as herpesviruses. The family name is derived from the Greek word herpein ("to creep"), referring to the latent, recurring infections typical of this group of viruses. Herpesviridae can cause latent or lytic infections.
General properties
HSV and transplantation; with short classification
Aggresomes and Autophagy Generate Sites for Virus Replication 2006
Strains
Metabolism
Herpesvirus assembly: a tale of two membranes 2006
Local
"Virus Receptors"
"Iron Deficiency ???"
"Acid Vesicles ??"
Diagram of herpesvirus assembly.
- Intranuclear capsids assemble around a scaffold (1–3), and DNA is packaged (4) into preformed capsids. DNA-containing capsids (5) contact the inner nuclear membrane at sites where the nuclear lamina has been locally dissolved (6), followed by budding at the inner nuclear membrane resulting in enveloped primary virions in the perinuclear cleft (7).
- The primary envelope fuses with the outer nuclear membrane (8), leading to translocation of the nucleocapsid into the cytosol where capsid-proximal tegument proteins assemble at the capsid (9), while at the final envelopment site, glycoproteins and outer tegument proteins gather (10).
- Both subassemblies then combine during secondary envelopment (11) and the enveloped virion is transported in a vesicle (12) to the plasma membrane for release (13).
- (10a–13a) Formation and release of capsid-less particles.
Viral proteins that have been discussed in the different steps are
- (1–3): pUL6, pUL18, pUL19, pUL26, pUL26.5, pUL35 and pUL38 (conserved);
- (4): pUL6 and pUL15–pUL28 (conserved);
- (6): pUL25, pUL31–pUL34 (conserved), pUS3 (α-);
- (8): pUL25 (conserved) and pUS3 (α-);
- (9): pUL36–pUL37 (conserved) and pUS3 (α-);
- (10): gM and pUL11 (conserved);
- (11): pUL48(α-).
Proteins with (α-) after them represent those that are found only in the Alphaherpesvirinae.
Competition for Iron
Iron metabolism markers and haptoglobin phenotypes in susceptibility to HSV-1 or/and HSV-2 lesion relapses. 2010
Fulltext
Hp 2.2 phenotype (that is associated with higher ferritin) may offer some protection against the recurrence of Herpes labialis or genitalis manifestations. The incidence of relapses is negatively correlated with serum ferritin
Patients with ferritin over 60/70 ug/L are usually asymptomatic (personal observation).
Kaposi Sarcoma
Localization
- Skin
- Mouth
- Genitalia
- Eye
- Sensitive Nerves
Clinical features
Varicella zoster virus infection: clinical features, molecular pathogenesis of disease, and latency.2008
The varicella zoster virus vasculopathies: clinical, CSF, imaging, and virologic features. 2009
Shift from latent to lytic phase
Host factors
Viral factors
HSV Lifecycle
Therapy
PERCHE’LE LESIONI DA HSV RICOMPAIONO SOTTO STRESS?
Neuroimaging of herpesvirus infections in children.2007
Inhibition of human herpes simplex virus type 2 by interferon gamma and tumor necrosis factor alpha is mediated by indoleamine 2,3-dioxygenase [4].
HSV and Cancer
Activation of Stat3 transcription factor by Herpesvirus saimiri STP-A oncoprotein. 2004
