Virologic and Immunologic Outcomes for HIV Patients With Coronavirus Disease 2019

Rong Hu, MPH; Han Yan, MPH; Manqing Liu, MSc; Li Tang, MPH; Wenhua Kong, MSc; Zerong Zhu, MSc; Pan Liu, MSc; Wenjuan Bai, MPH; Xuejiao Hu, MPH; Jie Ding, BD; Xia Wang, MPH; Nianhua Xie, MPH

Disclosures

J Acquir Immune Defic Syndr. 2021;86(2):213-218. 

In This Article

Discussion

We observed a greater number of males, underlying comorbidities of diabetes and hypertension, and older age in the 35 PLHIV coinfected with SARS-CoV-2. Those with severe COVID-19 may be more likely to have shortness of breath. Although we did not observe the role of other risk factors in the severe progression of COVID-19 among PLHIV as current literature found in general population.[10] The proportion of severe COVID-19 among PLHIV was much higher than that reported among general population in China (42.8% vs. 15.7%, P < 0.001).[11] However, the case fatality rate was comparable to that observed in general population with COVID-19[12] (5.7% vs. 5.0%, P = 0.694). It may be explained by the possibility that PLHIV had a deficient immune system and showed some persistent immune activation that may hinder the lethal progression of COVID-19 caused by severe cytokine storm.[11] Age, gender, and death rate we found were similar to those reported in PLHIV with COVID-19 in Madrid and Italy.[5,13]

Our data indicated that COVID-19 may put PLHIV at a risk for higher viral load despite continued ART against HIV infection, especially for those with severe/critical COVID-19. As we know, HIV could not be completely eliminated despite successful suppression of viral replication under ART, and it lurks in latent and active reservoirs.[14] CD8+ cells are required for maintenance of HIV viral reservoir suppression under ART.[15] However, CD8+ cells were gradually decreased with severity of COVID-19.[16] The source of the virus rebound in PLHIV may be probably the reactivation of virus transcription from a pool of latently infected cells, namely HIV latent reservoirs, after the depletion of CD8+ cells caused by infection of SARS-CoV-2.

Although both SARS-CoV-2 and HIV infection would lead to the decrease of CD4+ cell count, we did not find their additive effects on CD4+ cell count as we hypothesized. The reason remains unknown. We observed an insignificant decline of CD4+ cell count after COVID-19 among those with continuous ART against HIV infection. Whether continuous ART would play a significant role in maintaining stable immune status remains to be elucidated in further studies.

There are several limitations in our study. First, there is a lack of CD8+ measurement before COVID-19, so as to the CD4/CD8 ratio, which is also an important immunologic indicator in HIV infection and COVID-19. Second, we used a self-designed questionnaire to collect clinical findings related to COVID-19 because of limited access to relevant data in hospital, which may make our study susceptible to information bias. Third, there is a lack of treatment strategy for COVID-19, which may affect the observed outcomes in our study. Finally, because this is an observational study with small sample size in short time, the observed outcomes may need to be confirmed in larger cohort studies with longer observation time. However, given the short of data regarding the impact of COVID-19 on HIV progression, we believe that our data would provide useful information for concerning the management of PLHIV coinfected with SARS-CoV-2.

In conclusion, PLHIV coinfected with SARS-CoV-2 may be more likely to progress into severe COVID-19, but their risk of death is comparable to the general population with COVID-19. The coinfection of SARS-CoV-2 may put PLHIV at greater risk for HIV-1 viral rebound especially for those with severe/critical COVID-19, while having limited impacts on CD4+ cell count. Whether continuous ART against HIV infection would have significant impacts on CD4+ cell count among PLHIV coinfected with SARS-CoV-2 needs further research.

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