Association of Endothelial Dysfunction and Antiretroviral Therapy in Early HIV Infection.

Importance: Human immunodeficiency virus (HIV) infection is associated with increased cardiovascular disease (CVD) events. Endothelial dysfunction (EDF) is involved in CVD pathogenesis; however, EDF onset after HIV acquisition and the potential for reversibility with antiretroviral therapy (ART) have not been evaluated to date. Objective: To evaluate endothelial function with noninvasive reactive hyperemia index (RHI) in patients with early HIV infection at baseline and after ART initiation. Design, Setting, and Participants: Cohort study in which 61 members of the United States Air Force diagnosed with HIV infection from September 1, 2015, through September 30, 2017, were evaluated for baseline EDF. Natural log-transformed RHI values (lnRHI) of less than 0.51 and at least 0.51 were defined as abnormal and normal, respectively. The RHI interval changes were evaluated in a subgroup of 40 patients. Data were analyzed from September 30, 2017, through January 30, 2018. Exposure: Early HIV infection. Main Outcomes and Measures: Baseline EDF at HIV diagnosis and interval changes associated with ART initiation. Results: The 61 patients included in the analysis were predominantly male (58 [95%]) and mostly African American (35 [57%]), with a mean (SD) age of 28.1 (6.7) years at HIV diagnosis. Median time from estimated date of HIV seroconversion to RHI assessment was 10.6 months (interquartile range [IQR], 5.1-13.2 months), and the median CD4 lymphocyte count was 552/µL (IQR, 449/µL-674/µL). Patients had a mean (SD) body mass index of 26.2 (4.0), median (IQR) low-density lipoprotein cholesterol level of 97 (80-126) mg/dL, median (IQR) total cholesterol level of 163 (146-195) mg/dL, and no diabetes diagnoses. Overall mean (SD) lnRHI was 0.70 (0.29) at HIV diagnosis. Baseline RHI was normal in 47 patients (77%; mean [SD] lnRHI, 0.82 [0.20]) and was abnormal in 14 patients (23%; mean [SD] lnRHI, 0.30 [0.18]). Age (per 10-year increase) was not associated with an abnormal lnRHI (odds ratio, 2.15; 95% CI, 0.89-5.19; P = .09). Of the 41 patients with follow-up RHI assessments, 40 started ART immediately and repeated the RHI assessments at a median (IQR) of 6.4 (6.0-7.8) months. Use of ART was associated with an overall significan increase in mean (SD) lnRHI (0.13 [0.33]; P = .02). A greater increase in mean (SD) lnRHI was associated with abnormal (n = 11) compared with normal (n = 29) lnRHI at HIV diagnosis (0.33 [0.34]; P = .01 vs 0.04 [0.30]; P = .38). Among those with abnormal baseline lnRHI, 8 (73%) showed improved endothelial function after ART. The patient who declined ART converted from having a normal lnRHI (0.60) to an abnormal lnRHI (0.11) lnRHI after 8.3 months. Conclusions and Relevance: In this study, EDF was common in early HIV infection, with associated reversal in most patients taking ART. Results suggest that persistent EDF and CVD complications may be associated with delayed ART. Further studies are necessary to define the role of noninvasive endothelial function testing in patients with HIV infection.

Mucocutaneous Findings and Course in an Adult With Zika Virus Infection.

IMPORTANCE: The Zika virus epidemic has been declared a public health emergency of international concern by the World Health Organization. We describe the mucocutaneous features and histologic correlation in a patient with the acute Zika virus infection. OBSERVATIONS: We observed the presence of a diffuse papular descending eruption, petechiae on the palate, and hyperemic sclerae in a 44-year-old man returning from Puerto Rico with confirmatory testing for the Zika virus. CONCLUSIONS AND RELEVANCE: A detailed awareness of mucocutaneous findings associated with Zika virus infection will support its early recognition and will facilitate elimination of Zika infection from consideration for concerned patients who present with other, more common erythematous eruptions.

[Ocular manifestations of Ebola virus disease: What we learned from the last epidemic]. / Manifestations oculaires de la maladie à virus Ebola : les leçons de la dernière épidémie.

The Ebola virus disease (EVD) outbreak, which was declared as such in West Africa in March 2014, has become the largest EVD epidemic to date. It is the first time that EVD has been responsible for cases imported to the US as well as locally-acquired cases in Europe. Research on pathophysiology and treatment has been considerably accelerated, and more precise descriptions of various forms of ocular involvement have been obtained. Conjunctival hyperemia is often present during the acute phase, and it may contribute to the diagnosis of EVD in an epidemic context. During convalescence, ocular inflammatory manifestations may develop and can be caused by viral persistence in ocular tissue. Eye care providers need to be aware of the ophthalmic manifestations of EVD, sometimes several weeks after the acute infection, in order to recognize them and take appropriate safety precautions.

Human immunodeficiency virus per se exerts atherogenic effects.

OBJECTIVE: Premature atherosclerosis in HIV-infected patients has been attributed to highly active antiretroviral therapy (HAART) and the associated metabolic complications. Whether HIV per se plays a role is an unresolved issue. The purpose of this study was to evaluate whether HIV per se exerts atherogenic effects. METHODS: We measured carotid intima-media thickness (IMT) and brachial endothelial-dependent (FMD) and endothelial-independent (NMD) vasodilation in 38 naïve untreated HIV-infected patients and 41 healthy control subjects. RESULTS: Control subjects were selected as to match the HIV patients for metabolic risk factors. Mean carotid IMT was higher in HIV patients (0.85+/-0.2mm; p<0.001) than in controls (0.63+/-0.1mm). In a stepwise multiple regression model, the changes in carotid IMT were predicted by the duration of HIV infection (p<0.001) and CD4 T-cells (p=0.035). Brachial FMD was impaired in HIV patients (8.8+/-3% versus 12.2+/-3% in controls; p<0.001). In contrast, NMD values practically overlapped in the HIV patients and controls. Analysis of the data in relation to viral load showed that FMD was significantly more impaired in the subgroup of patients with viral load values above the median (p<0.001). In addition, there was a highly significant, inverse correlation between FMD and the HIV-RNA copies (p<0.001). CONCLUSION: HIV infection causes functional and structural vascular alterations in a very early stage of the infection independent of HAART and metabolic factors. The data lend support to the viral infectious theory of atherosclerosis. Early assessment of the vascular status in HIV-infected patients is suggested.