Herpes viruses envelope

Apoptotic cells overexpress PS in their plasma membranes, triggering their internalization. Viruses mimic apoptotic cells in this regard.

Inhibition by annexin V, a PS-binding molecule, is an indicator that viral envelope PS is important for viral entry Callahan et al. HSV-1 was incubated with soluble annexin V and tested for entry into cells that support known endocytotic or non-endocytotic entry routes for HSV.

These results suggest that PS is not critical for HSV entry, regardless of the cellular entry requirement of endocytosis or endosomal low pH. Virus was then pelleted to remove unbound annexin. At 6 to 8 h post-infection, beta-galactosidase activity of infected cell lysates was determined as an indicator of viral entry. Data are means of quadruplicate determinations with standard deviation. Cholesterol plays a key role in maintaining the integrity and stability of cellular membranes.

It may also help maintain the stability of HSV Viral infectivity was determined after each thaw. Taken together, the results suggest that envelope cholesterol is vital for the stability and infectivity of HSV Envelope cholesterol is critical for the stability of infectious HSV-1 particles. Data are the mean of triplicate determinations with standard deviation.

Viral membrane cholesterol facilitates the entry and infectivity of many enveloped viruses with some exceptions Campbell et al. HSV-1 propagated on cells containing the cholesterol precursor desmosterol was previously shown to be cholesterol-free, yet infectious Wudiri and Nicola, This suggests that the function s of cholesterol in the HSV-1 envelope, such as its role in fusion, can be performed by other sterols.

Cholesterol was not required for HSV-1 attachment to cells or for virus uptake from the plasma membrane by endocytosis. Cholesterol present in the host membranes is also important for HSV-1 membrane fusion Wudiri et al.

This contrasts with influenza membrane fusion, which only requires viral envelope cholesterol Sun and Whittaker, The role of cholesterol in membrane fusion including virus-mediated fusion has been studied for many years White and Helenius, ; Young et al.

Envelope cholesterol participates specifically in the membrane fusion function of several viruses Daya et al. How might cholesterol impact HSV-1 fusion? Conformational changes in gB are critical for HSV-1 membrane fusion. Interestingly, HSV envelope cholesterol is not required for the low pH-induced conformational changes in the antigenic and oligomeric structures of gB examined here, nor is it required for the reversibility of these changes Figure 5. During membrane fusion, cholesterol may promote viral membrane curvature and bending necessary for the merging of juxtaposed membranes.

Viral cholesterol removal negatively impacted HSV-1 entry regardless of whether entry proceeds by endocytosis or whether entry requires endosomal pH. Envelope cholesterol may serve a conserved function s in low pH-dependent and pH neutral fusion mechanisms. These viruses obtain their envelopes from the plasma membrane. HSV-1 derives its envelope from internal membranes, which tend to be less cholesterol-rich. It remains to be determined whether cholesterol-depleted HSV-1 can be successfully replenished.

We also provide evidence that viral cholesterol greatly influences the stability of infectivity of HSV Cholesterol may help maintain the integrity of the viral envelope allowing the particle to remain infectious for extended periods. Conceived and designed the experiments: GW and AN. Performed the experiments: GW. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Asher, Y.

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Cellular proteasome activity facilitates herpes simplex virus entry at a postpenetration step. Herpes simplex virus tegument ICP0 is capsid associated, and its E3 ubiquitin ligase domain is important for incorporation into virions. Dollery, S. Low pH-induced conformational change in herpes simplex virus glycoprotein B.

Low-pH-dependent changes in the conformation and oligomeric state of the prefusion form of herpes simplex virus glycoprotein B are separable from fusion activity. Eidelman, O. PubMed Abstract Google Scholar. Falke, D. Fusion from without induced by herpes simplex virus type 1.

Intervirology 24, — Geraghty, R. Entry of alphaherpesviruses mediated by poliovirus receptor-related protein 1 and poliovirus receptor. Science , — Increased expression of LDL receptor-related protein 1 during human cytomegalovirus infection reduces virion cholesterol and infectivity.

Cell Host Microbe 12, 86— Guyader, M. Role for human immunodeficiency virus type 1 membrane cholesterol in viral internalization. Huang, H. It infects human B-lymphocytes generally non-productive infection and epithelial cells productive infection.

It is linked with a wide range of diseases, including several different types of tumour. See links in the table for further information. EBV has also been associated with other diseases, including:. HHV-8 is detectable in Kaposi's sarcoma lesions.

HHV-8 may also be associated with [ 9 ] :. Take our quick 5 minute survey to share your thoughts on Patient. Herpesviridiae Taxonomy Browser. Clin Transl Immunology. All the Virology on the WWW. Neuropathol Appl Neurobiol. Lossius A, Johansen JN, Torkildsen O, et al ; Epstein-Barr virus in systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis-association and causation.

Int J Dermatol. N Engl J Med. Curr Infect Dis Rep. J Am Acad Dermatol. Mayo Clin Proc. Human Betaherpesvirinae include:. These herpesviruses are also lymphotropic and specific for either T or B lymphocytes.

Members of this subfamily isolated in humans are:. Recent research has uncovered the function or multiple functions of many herpesvirus genes, while some elude understanding and remain the focus of intense study. Other areas of current and future research include understanding the mechanisms for establishing, maintaining and reactivating latency, interactions between viral and host proteins and details of the variety of mechanisms involved in gene regulation. Herpesviruses are potential vectors for application to several problems in human health.

HSV-1 is a good candidate because it is possible to replace large segments of the genome with genes of choice. It's affinity for sensory nerves allows it to target gene therapy to the central nervous system, while it's capacity for cell destruction could be a powerful weapon for selective destruction of cancer cells.

An HSV-1 vector could be engineered to express antigens that induce immunity against a variety of infectious agents. Designing such vectors will require profound understanding of the herpesvirus genomes. Three recent publications contain both general and comprehensive reviws of the Herpesviridae family:. Sexually Transmitted Diseases , third edition , ed. Holmes et al. McGraw Hill. Peter E. Pertel, Patricia G.

Spear, chapt. Lawrence Drew, Michael P. Bates, chapt. Slobod, John W. Sixbey, chapt 23, "Epstein-Barr Virus Infection".