Background People with HIV (PWH) may have numerous risk factors for acquiring Coronavirus disease-19 (COVID-19) and developing severe outcomes, but current data are conflicting. Methods Healthcare providers enrolled consecutively by non-random sampling PWH with lab-confirmed COVID-19, diagnosed at their facilities between April 1st and July 1st, 2020. De-identified data were entered into an electronic Research Electronic Data Capture (REDCap). The primary endpoint was severe outcome, defined as a composite endpoint of intensive care unit (ICU) admission, mechanical ventilation, or death. The secondary outcome was the need for hospitalization. Results 286 patients were included; the mean age was 51.4 years (SD, 14.4), 25.9% were female, and 75.4% were African-American or Hispanic. Most patients (94.3%) were on antiretroviral therapy (ART), 88.7% had HIV virologic suppression, and 80.8% had comorbidities. Within 30 days of positive SARS-CoV-2 testing, 164 (57.3%) patients were hospitalized, and 47 (16.5%) required ICU admission. Mortality rates were 9.4% (27/286) overall, 16.5% (27/164) among those hospitalized, and 51.5% (24/47) among those admitted to an ICU. The primary composite endpoint occurred in 17.5% (50/286) of all patients and 30.5% (50/164) of hospitalized patients. Older age, chronic lung disease, and hypertension were associated with severe outcomes. A lower CD4 count (<200 cells/mm³) was associated with the primary and secondary endpoints. There was no association between the antiretroviral regimen or lack of viral suppression and predefined outcomes. Conclusion Severe clinical outcomes occurred commonly in PWH and COVID-19. The risk for poor outcomes was higher in those with comorbidities and lower CD4 cell counts, despite HIV viral suppression.

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As with many viruses, rabies virus (RABV) infection induces type I interferon (IFN) production within the infected host cells. However, RABV has evolved mechanisms by which to inhibit IFN production in order to sustain infection. Here we show that RABV infection of dendritic cells (DC) induces potent type I IFN production and DC activation. Although DCs are infected by RABV, the viral replication is highly suppressed in DCs, rendering the infection non-productive. We exploited this finding in bone marrow derived DCs (BMDC) in order to differentiate which pattern recognition receptor(s) (PRR) is responsible for inducing type I IFN following infection with RABV. Our results indicate that BMDC activation and type I IFN production following a RABV infection is independent of TLR signaling. However, IPS-1 is essential for both BMDC activation and IFN production. Interestingly, we see that the BMDC activation is primarily due to signaling through the IFNAR and only marginally induced by the initial infection. To further identify the receptor recognizing RABV infection, we next analyzed BMDC from Mda-5−/− and RIG-I−/− mice. In the absence of either receptor, there is a significant decrease in BMDC activation at 12h post infection. However, only RIG-I−/− cells exhibit a delay in type I IFN production. In order to determine the role that IPS-1 plays in vivo, we infected mice with pathogenic RABV. We see that IPS-1−/− mice are more susceptible to infection than IPS-1+/+ mice and have a significantly increased incident of limb paralysis.

Leukocyte migration and trafficking is dynamically regulated by various chemokine and adhesion molecules and is vital to the proper function of the immune system. We describe a role for the Cas and Hef-1-associated signal transducer in hematopoietic cells (Chat-H) as a critical regulator of T lymphocyte migration, by using lentivirus-mediated RNA interference (RNAi). Impaired migration of Chat-H-depleted cells coincided with defective inside-out signaling shown by diminished chemokine-induced activation of the Rap-1 GTPase and integrin-mediated adhesion. Localization of Chat-H to the plasma membrane, association with its binding partner Crk-associated substrate in lymphocytes (CasL), and Chat-H-mediated CasL serine-threonine phosphorylation were required for T cell migration. These results identify Chat-H as a critical signaling intermediate acting upstream of Rap1 to regulate chemokine-induced adhesion and migration.

BackgroundTraditional cardiovascular disease (CVD) risk factors contribute to increase risk of CVD in people living with HIV (PLWH). Of all world regions, sub-Saharan Africa has the highest prevalence of HIV yet little is known about PLWH’s CVD knowledge and self- perceived risk for coronary heart disease (CHD). In this study, we assessed PLWH’s knowledge, perception and attitude towards cardiovascular diseases and their prevention.MethodsWe conducted a cross-sectional study in the largest HIV care program in western Kenya. Trained research assistants used validated questionnaires to assess CVD risk patterns. We used logistic regression analysis to identify associations between knowledge with demographic variables, HIV disease characteristics, and individuals CVD risk patterns.ResultsThere were 300 participants in the study; median age (IQR) was 40 (33–46) years and 64 % women. The prevalence of dyslipidemia, overweight and obesity were 70 %, 33 % and 8 %, respectively. Participant’s knowledge of risk factors was low with a mean (SD) score of 1.3 (1.3) out of possible 10. Most (77.7 %) could not identify any warning signs for heart attack. Higher education was a strong predictor of CVD risk knowledge (6.72, 95 % CI 1.98-22.84, P < 0.0001). Self-risk perception towards CHD was low (31 %) and majority had inappropriate attitude towards CVD risk reduction.ConclusionDespite a high burden of cardiovascular risk factors, PLWH in Kenya lack CVD knowledge and do not perceived themselves at risk for CHD. These results emphasis the need for behavior changes interventions to address the stigma and promote positive health behaviors among the high risk HIV population in Kenya.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-015-1157-8) contains supplementary material, which is available to authorized users.