The association of HIV and cocaine use to cigarette smoking in the context of depression and perceived stress.

Mental well-being can contribute to cigarette smoking and negatively impact disease progression among people living with HIV (PLWH). This study examined potential associations between cocaine use (COC), depression, and HIV status in predicting cigarette smoking; hypothesizing that depression would be highest in cocaine users and predict cigarette smoking. An exploratory analysis including stress was also examined as a potential predictor of cigarette use. More than half of the sample (65%) endorsed smoking at some point in the past, and 52% endorsed being current smokers at the time of the study. Smokers were most likely to be cocaine users (87.1%), cocaine using PLWH (74.3%), or PLWH (36.6%). Neither HIV status (χ2(1) = 1.5, p = .221), perceived stress (χ2(1) = 0.75 p = .386), nor depressive symptomatology (χ2(1) = 1.2, p = .274) were related to smoking. Non-cocaine users were approximately 95.4% less likely to smoke than cocaine users, controlling for all other variables. Overall, cocaine use was the greatest predictor of cigarette smoking and quantity of cigarettes smoked. Perceived stress and depression were not associated with cigarette smoking in the sample. Future interventions targeting cigarette use should include a cocaine-related component to encourage smoking cessation among this high-risk group.

Fulminant hepatitis from herpes simplex virus type 2 in an immunocompetent adult.

Herpes simplex virus (HSV) is regarded as a common viral pathogen that produces a wide variety of diseases. After a primary infection, which usually occurs during childhood and may or may not be clinically evident, the virus establishes a latent infection in the local sensory ganglia and can reactivate throughout the life of the individual. Fulminant hepatic failure (FHF) due to HSV infection is a clinical condition well known in pediatric, immunocompromised, and pregnant patients. It is rare in immunocompetent hosts. We report the case of a 51-year-old man with no significant past medical history who developed FHF with disseminated intravascular coagulopathy and septic shock secondary to HSV infection. The initial diagnosis was made through a frozen section of a needle liver biopsy and the presence of HSV was confirmed in the permanent section with immunohistochemistry. HSV was grown in cell culture from liver tissue obtained through an autopsy.

Wernicke's encephalopathy in AIDS: a preventable cause of fatal neurological deficit.

Wernicke's encephalopathy is commonly associated with chronic alcohol abuse, but may also occur in patients with poor nutritional status. We report a case of acute Wernicke's encephalopathy in a patient with AIDS without any predisposing risk factors for thiamine deficiency. In developing countries, without vitamin supplementation, this disorder may play a role in the morbidity and mortality associated with AIDS. We believe that thiamine supplementation should be considered in cachetic AIDS patients, especially where access to antiretroviral therapy is limited.

Emergence of human immunodeficiency virus type 1 variants with resistance to multiple dideoxynucleosides in patients receiving therapy with dideoxynucleosides.

A set of mutations [Ala-62-->Val(A62V), V75I, F77L, F116Y, and Q151M] in the polymerase domain of reverse transcriptase (RT) of human immunodeficiency virus type 1 (HIV-1) confers on the virus a reduced sensitivity to multiple antiretroviral dideoxynucleosides and has been seen in HIV-1 variants isolated from patients receiving combination chemotherapy with 3'-azido-3'-deoxythymidine (AZT) plus 2',3'-dideoxycytidine (ddC) or 2',3'-dideoxyinosine (ddI). The IC50 values of AZT, ddC, ddI, 2',3'-dideoxyguanosine, and 2',3'-didehydro-3'-deoxythymidine against an infectious clone constructed to include the five mutations were significantly higher than those of a wild-type infectious clone. The K1 value for AZT 5'-triphosphate determined for the virus-associated RT from a posttherapy strain was 35-fold higher than that of RT from a pretherapy strain. Detailed analysis of HIV-1 strains isolated at various times during therapy showed that the Q151M mutation developed first in vivo, at the time when the viremia level suddenly increased, followed by the F116Y and F77L mutations. All five mutations ultimately developed, and the viremia level rose even further. Analyses based on the three-dimensional structure of HIV-1 RT suggest that the positions where at least several of the five mutations occur are located in close proximity to the proposed dNTP-binding site of RT and the first nucleotide position of the single-stranded template.