The present study examined neuropsychological (NP) functioning and associated medical, neurological, brain magnetic resonance imaging (MRI), and psychiatric findings in 389 nondemented males infected with Human Immunodeficiency Virus-Type 1 (HIV-1), and in 111 uninfected controls. Using a comprehensive NP test battery, we found increased rates of impairment at each successive stage of HIV infection. HIV-related NP impairment was generally mild, especially in the medically asymptomatic stage of infection, and most often affected attention, speed of information processing, and learning efficiency; this pattern is consistent with earliest involvement of subcortical or frontostriatal brain systems. NP impairment could not be explained on the bases of mood disturbance, recreational drug or alcohol use, or constitutional symptoms; by contrast, impairment in HIV-infected subjects was related to central brain atrophy on MRI, as well as to evidence of cellular immune activation and neurological abnormalities linked to the central nervous system. (JINS, 1995, 1, 231–251.)
The chemokine receptor CCR5 and to a lesser extent CCR3 and CCR2b have been shown to serve as coreceptors for human immunodeficiency virus type 1 (HIV-1) entry into blood- or tissue-derived macrophages. Therefore, we examined the expression of the chemokine receptors CCR1, CCR2b, CCR3, CCR5, and CXCR4 as RNAs or as membrane-expressed antigens in monocytes maturing into macrophages and correlated these results with the susceptibility of macrophages to HIV-1 infection, as measured by their concentrations of extracellular p24 antigen and levels of intracellular HIV DNA by quantitative PCR. There was little change in levels of CCR1, CCR2b, and CCR5 RNAs. CCR3 RNA and surface antigen were undetectable throughout maturation of adherent monocytes over 10 days. CXCR4 RNA and membrane antigen were strongly expressed in newly adherent monocytes, but their levels declined at day 7. The amounts of CCR5 RNA remained stable, but the amounts of CCR5 antigen increased from undetectable to peak levels at day 7 and then declined slightly at day 10. Levels of susceptibility to laboratory (HIV-1BaL) and clinical strains of HIV-1 showed parallel kinetics, peaking at day 7 and then decreasing at days 10 to 14. The concordance of levels of HIV DNA and p24 antigen suggested that the changes in susceptibility with monocyte maturation were at or immediately after entry and correlated well with CCR5 expression and inversely with CXCR4 expression.
This study considers the interrelationships among coping, conflictual social interactions, and social support, as well as their combined associations with positive and negative mood. Research has shown that each of these variables affects adjustment to stressful circumstances. Few studies, however, examine this full set of variables simultaneously. One hundred forty HIV-infected persons completed a questionnaire containing measures of coping, social support, conflictual social interactions, and positive and negative mood. Factor analyses showed that perceived social support and conflictual social interactions formed separate factors and were not strongly related. Compared to perceived social support, social conflict was more strongly related to coping behaviors, especially to social isolation, anger, and wishful thinking. Conflictual social interactions were more strongly related to negative mood than was perceived social support. Coping by withdrawing socially was significantly related to less positive and greater negative mood. The findings point to the importance of simultaneously considering coping, supportive relationships, and conflictual relationships in studies of adjustment to chronic illness. In particular, a dynamic may occur in which conflictual social interactions and social isolation aggravate each other and result in escalating psychological distress.
Objectives
To determine the prevalence and predictors of an incomplete immune response in patients with sustained viral suppression following their first or second combination antiretroviral treatment (cART) regimen.
Methods
All patients were recruited to the Australian HIV Observational Database (AHOD) by March 2006. Data were analysed to assess the prevalence of an incomplete immune response (<350 cells/μL) in the 12-24 months after starting the first or second cART regimen. Factors associated with an incomplete immune response were assessed using logistic regression and time to AIDS/death was assessed using survival analysis.
Results
Of the 2493 patients recruited to AHOD by March 2006, 590 were eligible for the analysis. Twenty eight percent of patients with a baseline CD4 count <350 cells/μL had an incomplete immune response 12-24 months after starting their first or second cART regimen. Lower baseline CD4 count prior to starting the cART regimen was predictive of an incomplete immune response. There was a non-significant trend towards faster AIDS or death in incomplete immune responders.
Conclusions
An incomplete immune response in patients with sustained viral suppression is associated with poorer immune function prior to starting cART. Type of cART or individual antiretroviral drugs was not associated with an incomplete immune response.
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