The main findings in the present study were a 6% prevalence of HIV-infected patients with COVID-19. HIV-infected patients were younger than HIV-uninfected patients by a decade. They were more likely to lack health insurance and to present with headache, productive cough, wheezing and abdominal pain than HIV-uninfected patients. While significant comorbidities among HIV-uninfected patients were diabetes mellitus and hypertension, a past history of tuberculosis and stroke were significant comorbidities among HIV-infected COVID-19 patients. HIV-infected patients significantly presented with high D-dimer and low hemoglobin levels.
The prevalence of HIV infection in our study was higher than that reported in a tertiary hospital in Nairobi, Kenya, which showed a 3.7% prevalence of HIV in COVID-19 patients25. Again, the prevalence of 6% is higher than the cumulative prevalence of HIV in Tanzania, estimated to be 4.7% in adults 31. The higher prevalence of HIV than the national prevalence likely suggests that HIV infection is a risk factor for SARS‑CoV‑2 infection. Unfortunately, we could not characterize these HIV-infected patients in terms of their VL and CD4 counts owing to the low numbers of HIV-infected patients who reported VL and CD4 counts.
Admitted HIV-infected patients in the present study were a decade younger than HIV-uninfected patients, suggesting that HIV infection is an independent risk factor for COVID-19. Lack of health insurance among HIV-infected COVID-19 patients is a proxy indicator for low socioeconomic status, which is known to be one of the risk factors for HIV infection 32,33.
Contrary to the findings of other studies that found no significant difference in the clinical presentation of COVID-19 between HIV-infected and HIV-uninfected patients 12–17, our study found that headache, productive cough, wheezing and abdominal pain were significantly higher among HIV-infected patients. This high prevalence of these symptoms could be due to the significant history of TB and previous stroke. HIV infection is known to be one of the risk factors for TB and neurological manifestations. 18,19 HIV patients with a prior history of TB may develop post-TB lung disease, which could have precipitated respiratory symptoms, and post-TB abdominal sequelae might have precipitated abdominal pain in HIV-coinfected COVID-19 patients. Again, headache could have been the sequelae of a previous history of stroke in our study patients.
Hypertension and diabetes mellitus were significantly lower in HIV-infected patients than in HIV-uninfected patients. Lower rates of hypertension and diabetes mellitus among HIV-infected patients were probably because of a younger age compared to HIV-uninfected patients. These findings differ from those of previous COVID-19 studies 9–11.
The duration of hospital stays among HIV-infected patients was comparable to that among HIV-uninfected patients. This similarity in hospital stay could exist because those with more severe disease would have died earlier and those who survived ended up having a similar duration of hospital stay as the HIV-uninfected group. A study in Kenya reported a similarity in the duration of hospital stay 25.
Furthermore, our study reported a significantly higher D-dimer level in HIV-infected patients than in HIV-uninfected patients. D-dimer is a specific fibrin degradation product (FDP) formed by plasmin degradation of cross-linked fibrin, not intact fibrinogen. This elevated D-dimer level can be attributed to increased reactive fibrinolysis, resulting in a hypercoagulable state and thrombotic events in both HIV and COVID-19. The hypercoagulable state and thrombotic events evidenced by higher D-dimer levels could also precipitate the headache, cough, wheezing and abdominal pain that we have seen in HIV-infected patients. The higher level of D-dimer reported in our study is also consistent with previous reports and further underscores the elevated risks of a hypercoagulable state and thrombotic events in HIV patients 34–36 and COVID-19 patients2,3,7.
Anemia was found to be significantly high in HIV-infected patients in our study. We attribute significant anemia in HIV-infected patients with COVID-19 to HIV infection or its treatment, as anemia is known to be associated with HIV infection and ART 37. In this study, we could not ascertain the ART regimen HIV patients were using. However, HIV-infected patients have been reported to have baseline anemia, an important predictor of anemia in the course of HIV infection 37
In the present study, a respiratory rate above 30 breaths per minute was significantly higher among HIV-infected patients than HIV-uninfected patients. A respiratory rate ≥ 30 breaths per minute is one of the criteria used to define the severity of COVID-19 27. Thus, the findings of the present study indicate that HIV coinfection results in severe COVID-19. This higher RR could be attributed to two factors. First, this could have been the past history of TB. TB sequela may cause chronic lung disease, which could cause severe COVID-19 among HIV-infected patients. Second, this could be due to a hypercoagulable state and thrombotic events evidenced by higher D-dimer levels, a proxy for pulmonary microembolism, which might cause respiratory distress manifested by a high RR.
Over half of HIV-infected patients died of COVID-19 compared to a third of HIV-uninfected patients. The higher mortality in HIV-infected patients could be attributed to disease severity. The high mortality rate of HIV-infected patients in our study seems more elevated than the results reported in previous studies 26,38–41. This high mortality could be due to the existence of important comorbidities among HIV-infected patients with previous stroke and past TB. TB sequela may cause chronic lung disease, which could contribute to succumbing to severe COVID-19 among HIV-infected patients.
The strength of this study is derived from its conduction in multiple centers across the country, thus having a national representation and a relatively larger sample size of HIV-infected patients with COVID-19 than the sample size in studies performed elsewhere 26,38–41.
A major limitation of this study is the reliance on reported HIV status and thus the presumption of contamination in both HIV-infected and uninfected groups of patients. Furthermore, the retrospective design of the study resulted in missing patient data on VL and CD4 counts. This might, in a way, affect the results of the present study.