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Herpetic simplex keratitis is a form of keratitis caused by recurrent herpes simplex virus (HSV) infection in the cornea. [ 1 ] It begins with infection of epithelial cells on the surface of the eye and retrograde infection of nerves serving the cornea. [ 2 ]
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]
During latency, most of the Herpes DNA is inactive, with the exception of LAT, which accumulates within infected cells. The region of HHV DNA which encodes LAT is known as LAT-DNA. After splicing, LAT is a 2.0-kilobase transcript (or intron ) produced from the 8.3-kb LAT-DNA.
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 ...
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)
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.
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).
HSV epigenetics is the epigenetic modification of herpes simplex virus (HSV) genetic code.. As of 2012, an estimated 3.7 billion people globally were infected with oral herpes simplex virus (HSV-1), and 417 million were living with genital herpes (HSV-2) worldwide (World Health Organization, 2018).