Bell's palsy is the most common cause of facial paralysis. Although it has been associated with diabetes mellitus, hypertension, pregnancy, and preeclampsia, the etiology of Bell's palsy remains unknown. The reactivation of latent herpes simplex virus (HSV) or varicella-zoster virus (VZV) with subsequent inflammation and entrapment of the facial nerve in the narrow labyrinthine segment has been implicated as a cause of facial paralysis, but the active role of these viruses in Bell's palsy is still discussed. This study quantified HSV-1 DNA, VZV DNA, and HHV-6 DNA in 95 saliva samples collected from patients within 48 hr from the onset of paralysis. HSV-1, VZV, and HHV-6 were detected in 13%, 3%, and 61% of patients, respectively. The detection rate did not differ significantly between patients and a control group of healthy donors. Interestingly, however, the value of HHV-6 DNA copies was significantly higher than that detected in healthy donors. In addition, the mean value of HHV-6 DNA recorded in patients who had at least a one grade improvement of palsy at the first visit was significantly lower than that detected in patients who showed no change in facial palsy grade or an increase of at least one grade. These findings call into question the role of HSV-1 and VZV in the etiology of Bell's palsy, and suggest that HHV-6 may be involved in the development of the disease or that the underlying disease mechanism might predispose patients to HHV-6 reactivation.

Human herpes viruses (HHVs) have been frequently detected in the gastrointestinal (GI) tract and may contribute to the development of gastric cancer. In the present study, the detection rate and viral load of Epstein Barr virus (EBV), HHV-6 and Cytomegalovirus (CMV) were assessed in the GI tract of human immunodeficiency virus (HIV) positive patients and of uninfected patients. The analysis revealed a significantly higher detection rate of EBV and HHV-6 in HIV-infected individuals than in uninfected subjects (88.5 vs 63%; p = 0.03). Moreover, EBV DNA load was significantly higher in the stomach of HIV patients than in controls. These data suggest that the HIV infection status may increase the persistence of these viruses in the GI compartment. Intriguingly, CMV DNA was undetectable in all biopsy specimens analyzed.

The distribution of antiretroviral (ARV) therapy resistance mutations among HIV-1 strains was evaluated in 39 postpartum women, one pregnant woman, and 12 HIV-positive babies (seven newborns and five children) living in rural west Cameroon. Thirty-five women and all newborns received a single dose of nevirapine (NVP) to prevent mother-to-child transmission of HIV-1; two women were ARV treated and three were ARV naive. Of the 52 viral strains examined, three were subtype B, 45 were classified into eight HIV-1 non-B subtypes, and four remained unclassifiable. Sequence analysis for genotypic drug resistance in the reverse transcriptase (RT) gene showed the presence of mutations associated with nonnucleoside RT inhibitor resistance in 20% of the samples from NVP-treated women and in 57% of those from treated newborns. Mutations associated with nucleoside RT inhibitors (M184V in one case and V118I in four cases) were found in five samples, despite being derived from ARV-naive patients. As expected, a greater frequency of mutations was found in the protease gene region. Of the sequences analyzed, 79% harbored five to seven specific mutations. The secondary mutations showed the typical protease inhibitor resistance-associated pattern for non-subtype B viruses, M36I being the predominant mutation (92.5% in women, 100% in babies). Other mutations frequently detected were K20I, L63P, H69K, and I13V. These findings confirm that resistance mutations can be detected in ARV-naive patients infected with non-B subtypes and emphasize an urgent need for studies assessing the impact of these mutations on the efficacy of subsequent ARV therapy and on the appearance of drug-resistant strains.

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