Severe coronavirus disease 2019 in a patient with HIV-2 infection.

Abstract

Around the globe, millions of people living with HIV-1 face the challenges posed to them by the current coronavirus disease 2019 (COVID-19) pandemic [1,2]. Thriving on health disparity, COVID-19 can overwhelm the same communities where HIV-1 prevalence is highest [3,4]. Despite the threat of insufficient public health support, it is vital to ensure a continuous provision of a good quality of care and the avoidance of treatment discontinuation [5]. Alarmingly, people living with an HIV-1 infection also seem to be at increased risk of COVID-19 mortality [3]. However, to the best of our knowledge, no data are available for people infected with HIV-2 infection. Here, we describe a unique case of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (the virus that causes COVID-19), infection in a patient who is being treated for HIV-2. In April 2020, a 66-year-old patient presented at the emergency room with a 5-day history of fever, dry cough and shortness of breath. The episode started with complaints of unsteadiness upon which he had fallen on the ground of his bedroom. A review of systems was negative for chest pain, rhinorrhoea, altered smell or taste, sore throat or any gastrointestinal symptoms. Born in Burkina Faso, he was living in the Netherlands since 15 years. He was known at our outpatient HIV clinic because of a well controlled asymptomatic HIV-2 monoinfection diagnosed in 2014 for which he received a fixed combination of darunavir/cobicistat/emtricitabine/tenofoviralafenamide. His plasma HIV-2 RNA load was less than 50 copies/ml with a CD4+ cell count of 760 × 106/l and a CD8+ cell count of 510 × 106/l. In addition, he was known with obesity (BMI 32.8 kg/m2) and moderately controlled hypertension treated with losartan and hydrochlorothiazide. On presentation, he was hypoxemic with a SpO2 of 90% on 5 l/min oxygen. His temperature was 38.0 °C and his respiratory rate was 30/min. Blood pressure and pulse were normal. On auscultation, bibasal crackles was heard. The patient's full blood count demonstrated a normal white cell count (8.5 × 109/l) with a diminished lymphocyte (1.42 × 109/l) and platelets count (104 × 109/l). Haemoglobin was 13.7 g/l and the d-dimer level was strongly elevated at 13.15 mg/l. Biochemical markers demonstrated raised levels of C-reactive protein (242.3 mg/l), aspartate aminotransferase (879 IU/l), alanine aminotransferase (134 IU/l), creatine (2.32 mg/dl) and creatine phosphokinase (40.724 U/l). Lactate (1.5 mmol/l) and bicarbonate (23.1 mmol/l) levels were normal. The patient underwent thoracic computed tomography (CT) which demonstrated widespread bilateral areas of patchy consolidations, findings consistent with severe COVID-19 infection (classified as CO-RADS 5 and CT severity score 7). An ultrasound for lower extremity deep venous thrombosis was negative. The nasopharyngeal SARS-CoV-2 PCR was positive. The patient was admitted to a COVID-19 ward and received treatment with oxygen and empiric broad-spectrum antibiotics according to the then current guidelines [1]. For the presumptive diagnosis of acute renal failure secondary to rhabdomyolysis fluid, resuscitation was started. After 6 days, he was discharged from the hospital in good health. All abnormal laboratory values continued to normalize. In addition to persistent but waning complaints of shortness of breath for a period of approximately 4 months, his recovery was otherwise uneventful. A follow-up CT-scan 4 months after his initial presentation showed a clear decline of COVID-19-related lung abnormalities. Total SARS-CoV-2 antibodies (including IgG and IgM) became positive (Wantai ELISA) and his plasma HIV-2 RNA load remains undetectable. Now, 8 months after his original presentation, he is in good spirits and does not experience any long-term COVID-19-related adverse health outcomes. In conclusion, we present a first case report of a SARS-CoV-2 and HIV-2 coinfection in a patient who needed hospital admission for severe COVID-19 and experienced long lasting but self-limiting symptoms after discharge. His disease course was complicated by acute renal failure secondary to rhabdomyolysis which has been associated with COVID-19 in both HIV-1 positive and negative patients [6,7]. Most probably, the kidney injury is caused by pneumonia-induced rhabdomyolysis and direct effects of SARS-CoV-2 on the renal parenchyma [6]. After its first recognition in 1985, HIV-2 is now seen throughout West Africa with an exceptionally high prevalence in Burkina Faso [8]. It is estimated that approximately 1–2 million people live with HIV-2 worldwide [9]. Reported numbers of HIV-2 infections, however, may be a significant underestimation of actual numbers due to unrecognized or undiagnosed infections [8,9]. Our current case report highlights the potential challenges associated with HIV-2 infection in the current COVID-19 pandemic. Acknowledgements W.J.W. is currently receiving a Vidi grant (#91716475) from the Netherlands Organization for Scientific Research (NWO). M.v.d.V. has received consultancy fees paid to his institution by Gilead, MSD, ViiV and research support from Gilead, MSD, ViiV, Abbvie. Conflicts of interest There are no conflicts of interest.