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Similar to other herpesviridae, the herpes simplex viruses establish latent lifelong infection, and thus cannot be eradicated from the body with current treatments. [ 63 ] Treatment usually involves general-purpose antiviral drugs that interfere with viral replication, reduce the physical severity of outbreak-associated lesions, and lower the ...
Herpes simplex virions. Herpes simplex virus 1 and 2 (HSV 1 and HSV 2) are part of the alpha subfamily of herpesviruses. The lytic phase of infection occurs within mucoepithelial cells while the latent infection of these cells occurs in neurons. These two viruses are the cause of oral and genital herpes. [4]
Lytic infection is sometimes known as "productive" infection. Latent cells harbor the virus for long time periods, then occasionally convert to productive infection which may lead to a recurrence of symptomatic Herpes symptoms. During latency, most of the Herpes DNA is inactive, with the exception of LAT, which accumulates within infected cells.
Site of Latency Means of Spread HHV‑1: Herpes simplex virus-1 (HSV-1) α (Alpha) Mucoepithelial: Oral and/or genital herpes, herpetic gingivostomatitis, pharyngitis, eczema herpeticum, herpetic whitlow, herpes simplex keratitis, erythema multiforme, encephalitis, as well as other herpes simplex infections: Neuron (sensory ganglia)
Herpesviruses may enter a latent stage, inactively infecting their human host. Since its discovery in 1993, this phenomenon has been found among all of the betaherpesviruses. [39] Other betaherpesviruses establish latency as a nuclear episome, which is a circular DNA molecule (analogous to plasmids).
An example of such a gene product is the latency associated transcripts (LAT) in herpes simplex virus, which interfere with apoptosis by downregulating a number of host factors, including major histocompatibility complex (MHC) and inhibiting the apoptotic pathway. [17] A certain type of latency could be ascribed to the endogenous retroviruses.