Key result
White adipose tissue serves as a reservoir for SARS-CoV-2, with adipogenic signaling and viral loads differing significantly between male and female mice during co-infection with Trypanosoma cruzi.
Why the study?
Post-COVID cardiac damage poses a threat for cardiomyopathy and heart failure, and COVID-19 cases are increasing where Chagas heart disease caused by Trypanosoma cruzi is a major comorbidity, but the mutual effects of these infections remain unclear.
In a mouse model, white adipose tissue acts as a reservoir for SARS-CoV-2, and sex-specific differences in adipogenic signaling may influence cardio-pulmonary pathology during coinfection with Trypanosoma cruzi.
Background Coronavirus disease-2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2; CoV2) is a deadly contagious infectious disease. For those who survived COVID-19, post-COVID cardiac damage poses a major threat for the progression of cardiomyopathy and heart failure. Currently, the number of COVID-related cases and deaths are increasing in Latin America, where a major COVID comorbidity is Chagas’ heart disease (caused by the parasite Trypanosoma cruzi ). Here, we investigated the effect of T. cruzi infection on the pathogenesis and severity of CoV2 infection and, conversely, the effect of CoV2 infection on heart pathology during coinfection. Methodology/findings We used transgenic human angiotensin-converting enzyme 2 (huACE2) mice infected with CoV2, T. cruzi , or coinfected with both in this study. Our study shows for the first time that white adipose tissue (WAT) serves as a reservoir for CoV2 and the persistence of CoV2 in WAT alters adipose tissue morphology and adipocyte physiology. Our data demonstrate a correlation between the loss of fat cells and the pulmonary adipogenic signaling (via adiponectin isomers) and pathology in CoV2 infection. The viral load in the lungs is inversely proportional to the viral load in WAT, which differs between male and female mice. Our findings also suggest that adiponectin-PPAR signaling may differently regulate Chagas cardiomyopathy in coinfected males and females. Conclusion We conclude that adipogenic signaling may play important roles in cardio-pulmonary pathogenesis during CoV2 infection and T. cruzi coinfection. The levels of adiponectin isomers differ between male and female mice during CoV2 infection and coinfection with T. cruzi , which may differently regulate inflammation, viral load, and pathology in the lungs of both the sexes. Our findings are in line with other clinical observations that reported that males are more susceptible to COVID-19 than females and suffer greater pulmonary damage.
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Dhanyalayam et al. (2021) studied SARS-CoV-2 and Trypanosoma cruzi co-infection (n=16). SARS-CoV-2 and Trypanosoma cruzi co-infection vs. Uninfected, SARS-CoV-2 alone, or T. cruzi alone was evaluated on Cardio-pulmonary pathology, viral load, and adipogenic signaling. White adipose tissue serves as a reservoir for SARS-CoV-2, with adipogenic signaling and viral loads differing significantly between male and female mice during co-infection with Trypanosoma cruzi.
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