Clinical features and outcome of HIV/SARS‐CoV‐2 coinfected patients in The Bronx, New York city

Abstract

Currently, coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a public health crisis, with almost five million people have been infected and of which more than 300 000 died.1 Older ages and several comorbidities, such as hypertension, diabetes mellitus, and cardiovascular diseases, are identified as risk factors for developing severe COVID-19 and deaths.2, 3 It is estimated that 40 million people worldwide have human immunodeficiency virus (HIV) infection.4 Thus, we are expecting to encounter a significant number of patients with HIV with SARS-CoV-2 infection. However, there is limited evidence regarding the impact of HIV infection on the severity and mortality related to COVID-19. Several case reports and case series showed that the mortality and severity of COVID-19 were not increased in patients with HIV.5-7 In contrast, HIV/SARS-CoV-2 coinfected patients may have mortality benefits from the immunosuppressive state.8 However, the data from our institution showed contradictory results. Herein, we presented the case series of hospitalized HIV patients with COVID-19 in a single hospital in the South Bronx, the area that is well known for its most poverty, least education, highest criminal, and poorest health outcomes in New York. The clinical features and outcomes of nine HIV/SARS-CoV-2 coinfected patients admitted to our hospital from 25 March to 20 April 2020 are discussed. Table 1 provides demographic data, clinical features, and outcomes of each patient. The median age of the patients was 58 years old (range, 31-76). Seven were males and two were females. All patients had multiple comorbidities. The diagnosis of COVID-19 was confirmed by a positive SARS-CoV-2 RT-PCR test from nasopharyngeal swab specimens. Most recent patients CD4+ T cell count ranged from 179 to 1827 per mm3. HIV viral load was very low to undetectable. Eight patients were on highly active antiretroviral therapy (HAART), of which six reported medication compliances. HAART was discontinued during hospital admission in four patients, two of which was due to acute kidney injury (AKI), and the other two were for an unclear reason. Fever, cough, and dyspnea were the most common presenting symptoms among all patients. One patient initially presented with gastrointestinal tract symptoms, including nausea, vomiting, and watery diarrhea. Chest X-ray (CXR) abnormalities compatible with COVID-19 pneumonia were found in eight patients (89%) and correlated with disease severity. All patients' blood cultures were negative. Seven patients eventually died (78%), of which four due to hypoxemic respiratory failure and three from septic shock and multiorgan failures. Recent evidence demonstrated that several clinical features, including older age, lymphopenia, elevated inflammatory markers, and CXR abnormalities are predictive factors for severe COVID-19 and death.2, 3, 9 We found a similar pattern in HIV/SARS-CoV-2 coinfected patients. Also, typical CXR abnormalities representing COVID-19 pneumonia were similar among all HIV patients regardless of their CD4 count. Compare to previous studies5-7; our patients had significantly lower CD4+ cells count but showed a higher mortality rate. The inverse relationship between CD4+ cell count and mortality rate contradicts the hypothesis that HIV/SARS-CoV-2 coinfected patients have favorable prognoses because of paradoxical prevention from robust cytokine storms due to their immunosuppressive states and HIV-related lymphopenia.8 Moreover, the extremely high mortality rate observed in our case series raises the concern that HIV infection and low CD4+ cell counts may negatively impact on COVID-19 outcomes. It was clear from our case series that immunocompromised state from HIV-related lymphopenia, unfortunately, cannot prevent against progression to severe COVID-19 and death, as opposed to B-cell suppression in some specific population, such as patients taking B-cell depleting medication.8-11 We proposed two possible explanations. First, host immunity response to SARS-CoV-2 requires T lymphocytes. HIV-related lymphopenia, therefore, delay the clearance of viruses and promote the progression of the disease. Second, the key pathogenesis of cytokines storms in severe COVID-19 may stem from the dysregulation of B lymphocytes so that HIV-related T-cell suppression does not confer any protective role against severe COVID-19. Our report had several limitations. First, the results were based on only nine patients. Second, all patients had several comorbidities that negatively impact the COVID-19 prognoses. Thus, further large observational studies are needed to verify our results. Understanding the clinical course and mechanism of COVID-19 in patients with HIV will help elucidate the pathogenesis of SARS-CoV-2 infection and the progression to severe disease, which will help in better management and prevention of COVID-19 in HIV patients and perhaps in general.

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