Recovery from COVID-19 following hepatitis C, human immunodeficiency virus infection, and liver transplantation.

To the Editor:

Immunosuppression and frequent comorbidities in transplant recipients potentially increase the risk of fatal outcomes of pandemic coronavirus disease 2019 (COVID‐19).

A 1965 born male had suffered from hemophilia A. In the 1970s, he acquired hepatitis C virus (HCV) infection, probably via factor VIII supplementation, and in 1985 human immunodeficiency virus (HIV) infection. Interferon‐based HCV therapy resulted in a sustained virological response. Antiviral treatment with emtricitabine/tenofovir alafenamide/rilpivirin for HIV is ongoing since 2016. HIV suppression with repeatedly negative PCR results has been achieved.

Liver cirrhosis was diagnosed in 2017. In 2018, a solitary hepatocellular carcinoma with a diameter of 55 mm was detected. After successful downstaging by transarterial chemoembolization, the patient underwent uneventful liver transplantation (LT) in January 2019. Initial immunosuppressive (IS) therapy consisted of tacrolimus, mycophenolate, and steroids. Steroids were ceased within 3 months. Check‐ups showed good graft function and general condition. One year after LT, HIV‐PCR was negative. CD4 cell count was 820/μL (normal 411‐1610), CD4/CD8 ratio was 3.16 (normal 1‐4.8).

On March 11, 2020, the patient met with friends, of which one had mild flu‐like symptoms. Twelve days later he developed fatigue and fever up to 39.6°C. He stayed at home and took paracetamol against the fever. On March 26, he went to the local hospital in order to be checked for COVID‐19. Following worsening symptoms and a positive result for SARS‐CoV‐2 PCR, he was hospitalized on April 2nd. The patient presented with fever (39.4°C), fatigue, cough, and tachycardia. Laboratory examination revealed moderate systemic inflammation with CRP 6.1 mg/dL (normal < 0.5), interleukin‐6 50.9 pg/mL (normal < 7), but normal procalcitonin and WBC. Aminotransferases were moderately elevated, synthetic liver function, and renal function were normal. Chest X‐ray showed diffuse bilateral infiltrates.

He received oxygen via nasal probe and ampicillin/sulbactam to prevent bacterial superinfection. No additional antiviral treatment was given. IS therapy was continued without changes. Fever ceased on day 3 of the hospital stay and symptoms gradually disappeared. Repeat SARS‐CoV‐2 PCR tested negative on April 8, and follow‐up chest X‐rays showed diminishing infiltrates. On April 9, he was discharged without fever and in good clinical condition. At a check‐up on May 15, flow cytometry showed normal CD4 cell count of 638/μl. HIV‐PCR had turned into slightly positive values (2.8 × 101 copies/mL).

Mortality rates of SARS‐CoV‐2 infection and COVID‐19 in LT recipients cannot be specified to date. Full IS therapy of the early postoperative period does not appear to be a risk factor of severe course, whereas age and metabolic risk conditions distinctly seem to predispose towards fatal outcome. Our patient does not show the common phenotype of metabolic syndrome. Maintenance of IS during COVID‐19‐illness has recently been recommended. A potential protective mechanism might be based on the properties of calcineurin inhibitors to reduce the production of cytokines such as interleukin‐6 and TNF‐α.

Whether long‐term HIV therapy had an influence on the outcome remains unclear. The moderate course and final recovery in a LT patient with complex virological history may be encouraging for patients and health‐care professionals.

DISCLOSURE

The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation.