Herpes simplex keratitis and steroids

Not only can herpes be spread if there is no sore, MOST herpes is transmitted in the absence of lesions! It is now estimated that over 80% of all genital herpes is transmitted when there isn't anything on the skin and no symptoms. Patients have been aware for many years that if they kissed someone while having a fever blister or had sex with their partner while having an outbreak of genital herpes that they were likely to transmit the virus. Despite this knowledge, however, a 30% increase in the prevalence of HSV 2 infections was documented in the 1980s and 1990s. This increase is most likely due to the presence of HSV on the genital skin in the absence of lesions or symptoms. This phenomenon is known as "asymptomatic viral shedding" and has been demonstrated in well-controlled clinical investigations. Most recently, persons who never recall having had an outbreak of genital herpes, but who have had positive blood tests for antibodies to herpes, also have been demonstrated to "shed" the virus occasionally from lips or genital skin. It has been demonstrated that persons who take acyclovir daily have reduced amounts of the virus in the absence of symptoms or lesions. The same is probably true of the newer drugs, famciclovir and valacyclovir. It is logical that taking one of these three drugs everyday would reduce the chances of passing the virus to an uninfected partner, but this has not yet been proven.

Current research is investigating therapeutic HSV vaccination strategies with the goal of inhibiting viral reactivation within the trigeminal ganglia and preventing reactivation events. CD8 T cells of the adaptive immune response function to inhibit viral reactivation within the trigeminal ganglion using non-lytic mechanisms. [33] Therefore, a therapeutic vaccine designed to boost the CD8 T cell response within latently infected ganglia may achieve inhibition of viral reactivation and subsequent corneal inflammation without the need for daily oral medication. Consistent with this hypothesis, a small controlled trial in humans demonstrated a significant reduction in HSV-1 ocular recurrences following subcutaneous administration of heat-inactivated HSV-1. [34] Although there was a trend toward decreased HSK recurrences in the vaccinated group, the study was not powered to achieve statistical significance for this subgroup of HSV ocular disease. Larger clinical trials are required to validate this very interesting finding.

Primary infection with HSV-1 occurs following inoculation of mucosal or skin surfaces by direct contact. Most ocular disease is thought to represent recurrent HSV disease following the establishment of viral latency in the host, rather than a primary ocular infection. Latency develops after the virus enters sensory neurons and travels to sensory ganglia (usually the trigeminal ganglion for ocular disease) by retrograde axoplasmic flow [ 3 ]. The virus remains in ganglia for the lifetime of the host. It has been proposed that HSV-1 latency may also be established in the cornea, although this is controversial [ 4-6 ]. (See "Pathogenesis of herpes simplex virus type 1 infection" .)

Newly identified T-cells, called CD8aa+ T-cells, are the first to contain the herpes virus before it erupts above the skin. Through new techniques, biopsies discovered these CD8aa+ T-cells were found where the dermis (outer layer of skin) and the epidermis (layer just below the surface) connect. This new discovery suggests that the recurrence of HSV-2 is in the skin and not in the ganglia. We hope to present the article in it's entirety soon.

Jia Zhu, Tao Peng, Christine Johnston, Khamsone Phasouk, Angela S. Kask, Alexis Klock, Lei Jin, Kurt Diem, David M. Koelle, Anna Wald, Harlan Robins, and Lawerence Corey Nature 497, 494-497 doi:/nature12110 (23 May 2013)  

Herpes simplex keratitis and steroids

herpes simplex keratitis and steroids

Newly identified T-cells, called CD8aa+ T-cells, are the first to contain the herpes virus before it erupts above the skin. Through new techniques, biopsies discovered these CD8aa+ T-cells were found where the dermis (outer layer of skin) and the epidermis (layer just below the surface) connect. This new discovery suggests that the recurrence of HSV-2 is in the skin and not in the ganglia. We hope to present the article in it's entirety soon.

Jia Zhu, Tao Peng, Christine Johnston, Khamsone Phasouk, Angela S. Kask, Alexis Klock, Lei Jin, Kurt Diem, David M. Koelle, Anna Wald, Harlan Robins, and Lawerence Corey Nature 497, 494-497 doi:/nature12110 (23 May 2013)  

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