Covid-19 and dengue: Double punches for dengue-endemic countries in Asia

Abstract

The coronavirus disease 2019 (Covid-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an international public health crisis with devastating effects. In particular, this pandemic has further exacerbated the burden in tropical and subtropical regions of the world, where dengue fever, caused by dengue virus (DENV), is already endemic to the population. The similar clinical manifestations shared by Covid-19 and dengue fever have raised concerns, especially in dengue-endemic countries with limited resources, leading to diagnostic challenges. In addition, cross-reactivity of the immune responses in these infections is an emerging concern, as pre-existing DENV-antibodies might potentially affect Covid-19 through antibody-dependent enhancement. In this review article, we aimed to raise the issue of Covid-19 and dengue fever misdiagnosis, not only in a clinical setting but also with regards to cross-reactivity between SARS-CoV-2 and DENV antibodies. We also have discussed the potential consequences of overlapping immunological cascades between dengue and Covid-19 on disease severity and vaccine development.

Keywords: ADE; Covid-19; SARS-CoV-2; cross-reactivity; dengue.

FIGURE 1

Pathophysiological similarities between DHF and Covid‐19. Plasma leakage, thrombocytopenia, and coagulopathy are the hematological hallmarks of DHF and Covid‐19. Both DENV and SARS‐CoV‐2 induce the activation of immune cells leading to the release of pro‐inflammatory cytokines such as TNF and IL‐6. This event promotes increased vascular permeability that leads to plasma leakage. In DHF cases, the destruction of platelets in the peripheral region by DENV has been suggested as the cause of thrombocytopenia which in the end culminates as coagulopathy, disseminated intravascular coagulation, and in some cases, resulting in the death. While thrombocytopenia was also evident in Covid‐19 patients, pathophysiological mechanisms on how such event has occurred remain to be elucidated. Current data indicating that endothelial damage coupled with platelet apoptosis and impaired bone marrow growth might be the drivers of thrombocytopenia and coagulopathy in SARS‐CoV‐2‐infected patients. The sequential pathophysiological process leads to the occurrence of DIC and the death of Covid‐19 patients remains to be demonstrated