Herpes Virus Family
Viruses

Author: Gianpiero Pescarmona
Date: 12/06/2007

Description

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

Comments
2009-02-22T23:54:35 - Gianpiero Pescarmona

The insulin degrading enzyme binding domain of varicella-zoster virus (VZV) glycoprotein E is important for cell-to-cell spread and VZV infectivity, while a glycoprotein I binding domain is essential for infection. 2009

Zoster: TNF-inibitori aumentano il rischio
I farmaci che inibiscono il TNF-alfa sono già stati associati a gravi complicazioni infettive, ed è stato dimostrato che anche il fuoco di Sant'Antonio va aggiunto a questa lista. Sulla base di ciò, si raccomanda un attento monitoraggio dei pazienti trattati con anticorpi monoclonali anti-TNF-alfa per la comparsa di segni e sintomi precoci di infezione da herpes zoster. Il fuoco di Sant'Antonio è una patologia neurocutanea prodotta dalla riattivazione del virus varicella-zoster, ed è caratterizzato da un doloroso rash cutaneo dermatomatoso vescicolare. Questa malattia rappresenta uno dei più comuni effetti collaterali riportati negli studi clinici sui TNF-inibitori: le sue complicazioni comprendono sovrinfezione batterica e nevralgia posterpetica, che possono causare una morbidità sostanziale. (JAMA. 2009; 301: 737-44 e 774-5)

The irreversible binding of amyloid peptide substrates to insulin-degrading enzyme: a biological perspective. 2008

Papers Herpes Zoster laryngitis

Herpes zoster laryngitis: case report and serological profile. 2007
Watelet JB, Evrard AS, Lawson G, Bonte K, Remacle M, Van Cauwenberge P, Vermeersch H.
Eur Arch Otorhinolaryngol. 2007 May;264(5):505-7
Department of Otorhinolaryngology and Head & Neck Surgery, Ghent University Hospital, Ghent, Belgium. jeanbaptiste.watelet@ugent.be

Compared to herpes zoster oticus, varicella zoster virus (VZV) reactivations in immunocompetent patients are rare in laryngeal region. Usually, associated vocal cord paralyses are reported. Herein is a case report of a patient with laryngeal zoster without any associated motor disorders. An attempt is made to assign the distribution of mucosal eruptions to the appropriate neuroanatomical structures. A description of the serological course of VZV IgM and IgG are provided. Vesicles were found on the left sensory distribution areas of the superior laryngeal nerve. VZV IgM and IgG antibodies reached their peak 1 month after initial symptoms. Attentive follow-up and no antiviral therapy were advocated because of the absence of any immune deficiency or endoscopic suspicion of malignancy. In this case of VZV reactivation in the sensitive area of the superior laryngeal nerve, serological profiles of VZV IgM and IgG were profoundly modified up to the f

Attachments
fileuserdate
HSV_finale.docgp26/09/2007
Herpesvirus_e_trapianti.pptgp05/12/2007
kaposi-700.gifgp15/10/2009
rr-CMV-700.gifgp15/10/2009
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