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Human CD300a is known to promote the infection by dengue and other enveloped viruses and is overexpressed on CD4+ T cells from HIV-1-infected patients. We found that infected CD4+RA− T cells from untreated HIV-1-infected patients were mostly CD300a+. Furthermore, CD300a expressing CD4+RA− T cells from healthy donors were significantly more infected by HIV-1 in vitro than CD300a− cells. CD300a might represent a biomarker of susceptibility to HIV-1 infection on memory CD4+ T lymphocytes.

[Abstract Objective] To compare the prognostic performance of liver biopsy with that of liver stiffness measurement (LSM) to predict survival and liver decompensations among HIV/hepatitis C virus (HCV)-coinfected patients., [Design] Retrospective cohort study., [Methods] Cohort of 297 HIV/HCV-coinfected patients, who underwent a liver biopsy and LSM separated by 12 months or less, followed in 10 Spanish tertiary care centers from December 2005 to December 2011 (median follow-up, 5 years; interquartile range, 4.2–5.4 years). Liver biopsies were staged following the Scheuer's score. LSM was obtained by hepatic transient elastometry. A survival analysis was carried out and the integrated discrimination improvement was computed to compare the ability of the survival models to predict outcomes. The incidence of death from any cause and of development of the first decompensation of cirrhosis was calculated., [Results] Overall mortality rate was 1.63 [95% confidence interval (CI) 1.06–2.49] per 100 person-years. The adjusted hazard ratio [AHR (95% CI)] of baseline fibrosis (per stage of fibrosis) was 1.52 (1.08–2.15, P = 0.017) and of LSM (per 5 kPa increase) 1.28 (1.12–1.46, P < 0.001). LSM including models yielded a performance 3.9% better than the liver biopsy-based models (P = 0.072). For the prediction of liver decompensations, the AHR (95% CI) of baseline fibrosis by liver biopsy (per stage of fibrosis) was 1.67 (1.15–2.43, P = 0.007) and of LSM (per 5 kPa increase) 1.37 (1.21–1.54, P < 0.001). LSM-based models yielded a performance 8.4% better than the liver biopsy-based models (P = 0.045)., [Conclusion] LSM-based prediction achieves a similar yield than liver biopsy-based models to predict overall mortality in HIV/HCV-coinfected patients. Models including LSM could predict better liver decompensations than liver biopsy.

Optimizing treatment for patients with persistent low-level viremia is complicated because most genotyping tests are validated for viral loads >1000 copies per milliliter. In this study, genotypes of 92 treatment-experienced patients with persistent low-level viremia were determined using an in-house assay. Based on the resistance profiles obtained from genotyping and patient pharmacologic history, patients were either maintained on their antiviral regimen (n = 51) or received an optimized regimen (n = 41). In the group receiving optimized treatment, undetectable viral loads were achieved in 73.2% at 6 months and at 90.2% at 1 year, indicating that treatment guided by genotyping of patients with low-level viremia is effective in achieving viral suppression.

Purpose of review: Insulin resistance, HIV, antiviral drugs and hepatitis C virus (HCV) infection contribute to a complex interaction involving the metabolic syndrome. The objective of this review was to explore the meaning of insulin resistance in HIV-HCV-coinfected patients and how it may impact on sustained virological response (SVR) and disease progression. Recent findings: In the HIV/HCV coinfection setting, insulin resistance seems to be associated with a reduction in rapid virological response and SVR to pegylated interferon and ribavirin, both in naive and treatment experienced patients. A recent meta-analysis demonstrated insulin resistance impairs SVR rate with an odds ratio 0.47 (95% confidence interval 0.31-0.71). However, many confounding factors may promote contradictory results. Prevalence of insulin resistance depends on surrogate markers of insulin resistance and the threshold for defining impaired insulin sensitivity. For example, homeostasis model for the assessment of insulin resistance may be influenced by both methods of insulin measurement and interpretation. Insulin sensitizers, lifestyle changes and improvement in the use of protease inhibitors should be evaluated in the management of coinfected patients. Summary: Insulin resistance is common finding in patients with HIV/HCV coinfection, with wide clinical consequences including progression of hepatic fibrosis and reduction in the response to antiviral treatment. Our understanding of this relationship continues to improve. More prospective studies are required to improve future management. © 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.