Exploring the Contrasts and Similarities of Dengue and SARS-CoV-2 Infections During the COVID-19 Era

Abstract

Extensive research has been conducted on the SARS-CoV-2 virus in association with various infectious diseases to understand the pathophysiology of the infection and potential co-infections. In tropical countries, exposure to local viruses may alter the course of SARS-CoV-2 infection and coinfection. Notably, only a portion of the antibodies produced against SARS-CoV-2 proteins demonstrate neutralizing properties, and the immune response following natural infection tends to be temporary. In contrast, long-lasting IgG antibodies are common after dengue virus infections. In cases where preexisting antibodies from an initial dengue virus infection bind to a different dengue serotype during a subsequent infection, there is a potential for antibody-dependent enhancement (ADE) and the formation of immune complexes associated with disease severity. Both SARS-CoV-2 and dengue infections can result in immunodeficiency. Viral proteins of both viruses interfere with the host's IFN-I signaling. Additionally, a cytokine storm can occur after viral infection, impairing a proper response, and autoantibodies against a wide array of proteins can appear during convalescence. Most of the reported autoantibodies are typically short-lived. Vaccines against both viruses alter the immune response, affecting the course of viral infection and enhancing clearance. A comprehensive analysis of both viral infections and pathogenicity is revisited to prevent infection, severity, and mortality.

Keywords: COVID-19; SARS-CoV-2 infection; antibodies; antibody-dependent enhancement (ADE); cytokine storm; dengue infection; platelets.

Figure 1

Comparison of the cytokine storm. The central circle represents a common pattern of cytokines observed in both dengue fever and SARS-CoV-2 infections. An uncontrolled inflammatory response leads to the concurrent release of elevated levels of various inflammatory cytokines, contributing to the pathogenesis associated with these infections. Numerous inflammatory cytokines and chemokines, including IL-6, IL-1β, IL-8, CCL8, CXCL9, CXCL16, MCP-1, and IP-10, as well as immunosuppressive cytokines, are notably elevated and correlate with the clinical severity of the disease. Although both viral infections, dengue and COVID-19, are characterized by a cytokine storm and multiorgan involvement, their pathogenesis, disease progression, and recovery processes differ significantly.

Figure 2

Antibody kinetics following initial viral infection. This figure illustrates the dynamics of antibody production during the first viral infections. IgM antibodies targeting dengue viral proteins exhibit longer persistence than those directed against SARS-CoV-2 proteins. IgG antibodies against SARS-CoV-2 demonstrate a decline after four weeks; conversely, antibody titers in dengue infections decrease at a significantly slower rate over time. This figure was created using BioRender^® software.

Figure 3

Differences in IgM and IgG kinetics in the second infection with dengue virus or SARS-CoV-2. On the left, the short time of IgM and the rapid and marked increase in IgG can be observed. In contrast to SARS-CoV-2 infection, IgM antibody timing differs, and IgG titers are relatively short lived. This figure was produced with the BioRender^® software.

Figure 4

Antibody-dependent enhancement in dengue and SARS-CoV-2 infection. Antibody-dependent enhancement (ADE) occurs when antibody–virus complexes are internalized into cells through FcγRs, resulting in the infection of a more significant number of target cells. This process may lead to increased viral production. ADE in dengue infection has been proven. In SARS-CoV-2 infection, there are still controversies; however, several receptors and co-receptors for SARS-CoV-2 entrance to the cells have been proven and illustrated before [42]. This figure illustrates the proposed mechanism. This figure was made using the BioRender^® software.