PubMed · 8657231
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S D Shafran. 1996-07-18. Herpes simplex encephalitis.. https://doi.org/10.1056/nejm199607183350316
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Acyclovir or similar agents with activity against Epstein-Barr virus (EBV) theoretically may prevent non-Hodgkin's lymphoma (NHL) in AIDS. A case-control study of 29 patients with AIDS-related NHL and 58 matched control subjects assessed the frequency with which daily acyclovir (>/=800 mg/d) or similar agents were used for > or =1 year. In a historical cohort of 304 patients with AIDS for > or =2 years, the prevalence of NHL was assessed among 3 groups of patients: those who received long-term treatment with high-dose acyclovir (or similar agents) or low-dose or intermittent acyclovir; those treated with ganciclovir/foscarnet for <1 year; and those who had not previously been treated with acyclovir, ganciclovir, or foscarnet. In the case-control study, 22 patients (72.4%) with NHL never received acyclovir or similar drugs versus 19 control subjects (32.8%; P=. 002); 2 patients (6.9%) with NHL received acyclovir (> or =800 mg/d) for > or =1 year versus 27 (46.6%) of control subjects (P=.0001). In the cohort study, 6 (6.8%) of 88 patients who received acyclovir (> or =800 mg/d) for > or =1 year developed NHL versus 15 (15.5%) of 97 patients who received intermittent or lower-dose acyclovir and 30 (25.2%) of 119 patients who never received these agents (P=.002). Long-term administration (>1 year) of high-dose acyclovir or similar agents with anti-EBV activity may prevent NHL in patients with AIDS. A prospective, randomized study is warranted to confirm these results.
Herpes zoster (commonly referred to as "shingles") and postherpetic neuralgia result from reactivation of the varicella-zoster virus acquired during the primary varicella infection, or chickenpox. Whereas varicella is generally a disease of childhood, herpes zoster and post-herpetic neuralgia become more common with increasing age. Factors that decrease immune function, such as human immunodeficiency virus infection, chemotherapy, malignancies and chronic corticosteroid use, may also increase the risk of developing herpes zoster. Reactivation of latent varicella-zoster virus from dorsal root ganglia is responsible for the classic dermatomal rash and pain that occur with herpes zoster. Burning pain typically precedes the rash by several days and can persist for several months after the rash resolves. With postherpetic neuralgia, a complication of herpes zoster, pain may persist well after resolution of the rash and can be highly debilitating. Herpes zoster is usually treated with orally administered acyclovir. Other antiviral medications include famciclovir and valacyclovir. The antiviral medications are most effective when started within 72 hours after the onset of the rash. The addition of an orally administered corticosteroid can provide modest benefits in reducing the pain of herpes zoster and the incidence of postherpetic neuralgia. Ocular involvement in herpes zoster can lead to rare but serious complications and generally merits referral to an ophthalmologist. Patients with postherpetic neuralgia may require narcotics for adequate pain control. Tricyclic antidepressants or anticonvulsants, often given in low dosages, may help to control neuropathic pain. Capsaicin, lidocaine patches and nerve blocks can also be used in selected patients.
Acyclovir resistance is not a recognized problem among neonates with perinatal herpes simplex virus (HSV) infection. A premature newborn with neurocutaneous HSV infection was treated for 21 days with acyclovir. Disseminated disease recurred 8 days later. A recurrent isolate was resistant to acyclovir and lacked thymidine kinase activity on the basis of a frameshift mutation in the thymidine kinase (tk) gene. Compared with the sensitive isolate obtained during primary infection, replication of the resistant isolate was reduced on primary and permanent cells and even further impaired on cells deleted for cellular tk. The resistant isolate lacked virulence in a murine model of genital infection. Acyclovir-resistant HSV-2 mutants can develop rapidly in neonatal infection and cause clinically significant disease, despite decreased replication in vitro and attenuated virulence in an animal model.