Herpesvirus 6 HHV

Over 20 infectious agents have been incriminated as etiologic agents for many the causal relationship has been disproved, and for others there is conflicting evidence. Human herpesvirus 6 (HHV-6) is currently the most likely causative virus. HHV-6 may initiate the autoimmune processes of MS in one of two ways. First, HHV-6 is structurally similar to myelin basic protein. When T cells become sensitive to HHV-6, the cells may attack myelin basic protein. Second, HHV-6 may directly stimulate the complement cascade, activating autoimmune processes.5 Infection with HHV-6 alone cannot fully explain MS, because HHV-6 is found in 75% of all people, but MS is much more rare. 

Acyclovir (Figure 49-2) is an acyclic guanosine derivative with clinical activity against HSV-1, HSV-2, and VZV, but it is approximately 10 times more potent against HSV-1 and HSV-2 than against VZV. In vitro activity against Epstein-Barr virus (EBV), cytomegalovirus (CMV), and human herpesvirus-6 (HHV-6) is present but weaker. 

A particular hepatotropicity causing severe herpes hepatitis is ascribed to herpesvirus 6 (HHV-6). There have even been reports of a fulminant course with this virus infection. (18, 23, 35) HHV-8 causes Kaposi s sarcoma. The liver is the most common site, with dark reddish-violet tumour nodes. Histological analysis reveals endothelial cell proliferations and growths of spindle-shaped fibroblast-like cells. The bile ducts may be altered. Transaminase levels are elevated, and jaundice occurs. There may be a causal relationship between HHV-8 infection and multicentric Castlemans disease. The latter usually implies the presence of peliosis hepatis, perisi-nusoidal fibrosis and nodular regenerative hyperplasia. 

In a non-randomized multicenter study of pre-emptive foscarnet sodium 90 mg/ kg/day in the prevention of human herpesvirus-6 (HHV-6) encephalitis in 21 allogeneic hemopoietic stem cell transplant recipients, the plasma HHV-6 DNA exceeded 5 x 10 copies/ml in eight patients [9 ]. The dosage was increased to 180 mg/ kg/day if the plasma HHV-6 DNA copy number increased to above 1 x 10 /ml or if... 

Herpesvirus 6 (HHV 6) is the etiologic agent for exanthema subitum, a common fever and rash syndrome of childhood. Rarely, HHV-6 causes bone-marrow suppression, pneumonia, or encephalitis. HHV-6 encodes a chemokine homologue named U83, which induces chemotaxis of the monocytic cell line THP-1 (Zou et al, 1999). It is still unclear whether the infected cells secrete this chemokine, but because the virus typically infects monocytes, U83 is hypothesized to be important for viral dissemination. 

Carbocyclic gnanosine analogues have been described to inhibit HSV-1, HSV-2, VZV, CMV, and/or other herpesviruses [viz. HHV-6 (human herpesvirus type 6)],... 

There are eight members of the herpesvirus family able to infect humans HHV-1 (herpes simplex virus 1, HSV-1) HHV-2 (herpes simplex virus 2, HSV-2) HHV-3 (varicella zoster virus,VZV) HHV-4 (Epstein-Barr virus, EBV) HHV-5 (cytomegalovirus, CMV) HHV-6 (human B-cell lymphotrophic virus or roseolovirus) HHV-7 (closely related to HHV-6) HHV-8 (a type of the rhadinovirus). 

HHV-6 (/3 herpesvirus) CC chemokine Sequence similarity no known function as yet... 

Various viruses encode proteins with sequenee homology to host proteins which are known to be involved in host defense functions. Viruses pirate and modify key immunoregulatory molecules, by use of molecular mimicry, to elude the Immune system (Murphy, 1997). Viruses also encode proteins that exploit or alter their host cells, replicate or induce migration for virus dissemination. Interestingly, DNA viruses such as the Herpesviruses (Cytomegalovirus (CMV), human herpesvirus (HHV-6 and 7), herpesvirus Saimiri (HVS) and Kaposi s sarcoma-associated Herpesvirus (KSHV)) all express GPCRs (Table 2). 

Acyclovir s clinical use is limited to herpesviruses. Acyclovir is most active against HSV-1, approximately half as active against HS V-2, a tenth as potent against vaiicella-zoster virus (VZV) and Epstein-Barr virus (EBV), and least active against cytomegalovirus (CMV) and human herpesvirus (HHV-6). Uninfected mammalian cells generally are unaffected by high acyclovir concentrations. 

Ogata M, Satou T, Inoue Y, Takano K, Dcebe T, Ando T, et al. Foscamet against human herpesvirus (HHV)-6 reactivation after aUo-SCT breakthrough FlFlV-6 encephalitis following antiviral prophylaxis. Bone Marrow Transpl 2013 48(2) 257-64. 

Viral particles of HCMV and Kaposi s sarcoma-associated herpesvirus/human herpesvirus 8 (KSHV/HHV-8) have recently been examined. During the her-pesviral replicative cycle, different viral particles are formed. For HCMV, this includes mature, infectious virions, noninfectious enveloped particles, and dense bodies [6]. Similarly for KSHV, only a portion of the produced virus particles is infectious [40]. Therefore, analysis of infectious virions requires their separation from the noninfectious and immature forms. Density ultacentrifugation gradients are typically used to separate the various forms. Each fraction can be analyzed by electron microscopy to determine the level of purity [6,41] or by assaying for viral DNA and an envelope glycoprotein [40]. 

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