12 octobre 2020 Articles scientifiques

Source : J Acquir Immune Defic Syndr  Volume 85, Number 2, October 1, 2020

Auteur : Smitha Gudipati, Indira Brar, Shannon Murray, John E. McKinnon, Nicholas Yared, and Norman Markowitz


BACKGROUND

COVID-19 disease has spread globally and was declared a pandemic on March 11, 2020, by the World Health Organization. On March 10, the State of Michigan confirmed its first 2 cases of COVID-19, and the number of confirmed cases has reached 47,182 as of May 11, 2020, with 4555 deaths.

INTRODUCTION

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a novel coronavirus first detected in December 2019 in Wuhan, Hubei Province, China.1 Many of the initial cases had a common exposure to the Huanan Wholesale Seafood Market that also traded live animals.2 SARS-CoV-2 was then identified on January 7, 2020, by the Chinese Center for Disease Control and Prevention, which then disclosed the genomic sequence on January 11, 2020.3 The World Health Organization named the infection caused by SARS-CoV-2, COVID-19. Since the initial detection of COVID-19, the disease has spread globally and was declared a pandemic on March 11, 2020, by the World Health Organization.4 In the United States, Detroit, Michigan, had become a “hotspot” of COVID-19 infected patients with the number of confirmed cases reaching 47,182 as of May 8, 2020, with 4555 deaths in Michigan (fourth most deaths in the United States).5 Currently, little is known if patients living with HIV (PLWH) are at a higher risk of severe COVID-19 or if antiretroviral medications used to treat HIV are protective against severe COVID-19. Tenofovir has been shown in vitro to tightly bind to the SARS-CoV-2 RNA-dependent RNA polymerase.6 Alternatively, lopinavir–ritonavir has already been shown to have no benefit beyond standard care in a large randomized control trial.7,8 In addition, little is known if and how frequently PLWH mount the intense cytokine response leading to cytokine storm and severe COVID-19. We describe our single-center experience in Detroit, Michigan, of COVID19 in patients infected with HIV-1. We reviewed patients’ demographics, clinical characteristics of both their HIV and COVID-19 coinfections, the antiviral and antiretroviral treatments they received, and their clinical outcomes.


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12 octobre 2020 Articles scientifiques

Source : AIDSNovember 01, 2020 – Volume 34

Auteur : Yousaf B. Hadi , Syeda F.Z. Naqvi , Justin T. Kupec and Arif R. Sarwari


OBJECTIVE

We studied clinical outcomes of COVID-19 infection in patients living with HIV (PLH) in comparison to non-HIV population.

INTRODUCTION

Severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) related disease (COVID-19) has emerged as the major health crisis of 2020 [1]. Its impact on patients with preexisting infection with HIV has hitherto not been studied extensively. Recently, the Centers for Disease Control and Prevention (CDC) highlighted that patients living with HIV may be at a heightened risk of severe illness from SARS-CoV-2 as compared to the general population [2]. This postulated increased risk was attributed to both biological immune compromise and comorbidities as well as socially produced burdens. However, others have suggested that the use of antivirals in this population may confer relative protection from the virus [3]. Considering the large global burden of patients living with HIV, data on COVID-19 infection in these patients are scarce and are limited to case reports and small case series, which do not allow for comparison of outcomes with non-HIV populations [4,5]. We aimed to utilize a multicentre research network to study outcomes in patients with COVID-19 with preexisting HIV infection in comparison to those without HIV coinfection.


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