Herpes simplex virus type 2 meningoencephalitis resistant to acyclovir in a patient with AIDS

Article Abstract:

Patients with human immunodeficiency virus (HIV) infection have suppressed immune systems and are thus at risk for the development of opportunistic infections. Herpes simplex virus (HSV) can infect patients with HIV. HSV type 1 (HSV-1) is associated with the development of cold sores or fever blisters, while HSV type 2 (HSV-2), also called genital herpes, is usually sexually transmitted and produces genital lesions. HSV-1 is the most neurotoxic form of HSV, and it can infect the central nervous system (CNS) and cause encephalitis (inflammation of the brain). HSV-2 infections in the CNS are rare. Acyclovir is a common antiviral drug used in AIDS patients to prevent opportunistic infections such as HSV. In order for acyclovir to work it must be activated by an enzyme called thymidine kinase (TK) which is present in the virus. In some cases a mutant strain of virus lacking the TK enzyme may appear, in which case the virus will be resistant to treatment with acyclovir. Previous studies have documented cases of HIV patients with acyclovir-resistant HSV skin lesions. Recently, a case of HSV-2 infection in the CNS of a patient with HIV was reported. This article describes the case of a 28-year-old homosexual male with AIDS who developed HSV-2 infection that caused sores around his rectum. During acyclovir treatment he developed meningoencephalitis (inflammation of the brain and its surrounding membranes). A brain biopsy sample showed the presence of HSV-2 that was sensitive to acyclovir. However, the infection was not responding to acyclovir treatment. Dual treatment with acyclovir and vidarabine was begun. Following a progressive relapse the patient died. A sample of spinal fluid, obtained by spinal tap, revealed the presence of acyclovir-resistant HSV-2. The HSV-2 infecting the CNS had become deficient in TK and thus developed resistance to acyclovir treatment. It is concluded that certain HSV-2 strains may be more neurovirulent (able to attack the nervous system) than had previously been expected, and that the resistance to acyclovir may have been the cause of death in this case study. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment, Development and progression, AIDS patients, Drug resistance in microorganisms, Microbial drug resistance, Opportunistic infections, Meningoencephalitis

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Capsaicin interferes with the centrifugal spread of virus in primary and recurrent genital herpes simplex infections

Article Abstract:

Herpes simplex virus (HSV) spreads within the body by virtue of its ability to be transported in neurons (nerve cells). There are two types of neuronal transport. Anterograde transport involves the transport of substances from the cell body of the neuron to the nerve terminal (ending), and retrograde transport involves the transport of substances from the nerve terminal to the cell body. HSV travels by retrograde transport from its site of inoculation (point of entry in the body) to sensory ganglia (clusters of nerve cell bodies), and then spreads throughout the body by anterograde transport to peripheral nerve endings. Studies performed in guinea pigs have shown that after vaginal inoculation with HSV, the virus is transported from ganglia in the vaginal area to the spinal cord and from the spinal cord to the skin, where it causes lesions or sores. Capsaicin (the hot substance in chili peppers) is toxic to sensory nerve fibers and inhibits neuronal transport. Therefore, recent studies have focused on the use of capsaicin to prevent the spread of HSV along sensory nerve fibers. Female guinea pigs were treated with capsaicin (125 mg/kg) and then inoculated intravaginally with HSV. Control animals received HSV without capsaicin. Three to four days after inoculation, all animals in the control group had skin lesions. The number and severity of the skin lesions were significantly reduced in the capsaicin-treated group. However, capsaicin did not prevent HSV replication in the vagina or the occurrence of genital lesions. It is concluded that capsaicin interferes with the anterograde transport of HSV and thereby reduces skin lesions. Future tests with other selective pharmacological agents may aid in defining the development of neurological viral infections and in controlling diseases. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Disease transmission, Herpes genitalis, Genital herpes, Capsaicin

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Protection against zosteriform spread of herpes simplex virus by monoclonal antibodies

Article Abstract:

Infection with herpes simplex virus (HSV-1) stimulates an immune response, which involves activation of T cells to kill the virus and activation of B cells to produce antibodies against the virus. At the site of the initial skin infection, HSV-1 spreads to the nervous system, from which it travels to other parts of the body and reappears as an infected skin lesion (open wound). When an infection spreads by way of the nervous system it is referred to as zosteriform spreading. The effectiveness of monoclonal antibodies (antibodies derived from a single cell) in preventing the zosteriform spread of HSV-1 infection was evaluated in mice. Two hours prior to inoculation with HSV, the mice were treated with several different types of monoclonal antibodies that would recognize and interact with different HSV-1 proteins, known as gB, gC and gD. The mice treated with monoclonal antibodies that recognize gC and gD HSV proteins had significantly fewer skin lesions than the untreated mice. The results suggest that these monoclonal antibodies are effective in reducing the zosteriform spread of HSV infection. The monoclonal antibodies may provide protection against the zosteriform spread of HSV by directly interacting with HSV (neutralization), by activating specific cells to destroy HSV (antibody-dependent cellular cytotoxicity), or both. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models, Evaluation, Monoclonal antibodies

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