PMC:7736111 / 93217-101529
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7736111","sourcedb":"PMC","sourceid":"7736111","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7736111","text":"Antibody Dynamics in COVID-19\nAntibody-based therapy is being considered as a potential intervention for COVID-19, owing to the successful preliminary results with CPT. However, this treatment approach may be associated with the risk of exacerbating COVID-19 severity, based on the experience from previous viral infections (Salazar et al., 2017). Further, like previous SARS-CoV infections, antibody response may not always favor viral clearance, instead of contributing to the underlying immunopathology in some instances (Zhang et al., 2006; Newton et al., 2016). This immunopathological state may thus attribute to factors such as robust and unregulated activation of B cells, ADE, presence of cross-reactive but non-neutralizing antibodies, and failure to mount a controlled B cell response. Across studies, higher antibody titers detected in patients with severe and critical condition in comparison to non-severe cases (Long et al., 2020a; Gudbjartsson et al., 2020; Zhao et al., 2020). One can argue that higher antibody titer should be beneficial to provide an adequate antiviral response but can be countered by the finding that higher antibody titers found in a large number of severe cases and patients requiring ventilation (Kaneko et al., 2020). This contradiction is yet to resolve, and the emerging data suggest that higher antibody response may reflect the over-activation and uncontrolled B cell response. Zheng M. et al. (2020) showed the presence of RBD-specific IgG and IgA antibodies in patients with severe disease condition. The study included 13 severe and 41 non-severe cases of various age groups.\nAlong with increased IgG and IgA levels, severe cases also had an increased number of antibody-secreting cells and TFH cells, which aid in antibody production. Further, a close correlation of proinflammatory cytokines and chemokines like IL-6, CXCL10 and complement activation marker C5a found with the severe disease condition. This study provided a direct relation of inflammatory response with humoral immune response in context to the disease severity. However, the antigen-neutralizing property of these SARS-CoV-2 specific antibodies was not determined. Further, a low sample size of severe cases was another limiting factor to provide a definitive conclusion that robust antibody response may positively correlate with disease severity.\nSimilarly, Zhao et al. (2020) studied antibody response in 173 clinically diagnosed COVID-19 patients with a median age of 48 years. Among these, nine patients (three critical and six non-critical) studied longitudinally for the relation of antibody response with the disease severity. Antibody titer was higher in the critical patients as compared to non-critical. This higher titer of antibodies was not reflected by the clearance of the virus, thus suggesting that antibody response in critical cases may be associated with worse disease outcome rather than protective effect. However, like other studies, this study also suffers from the same limitation of low sample size. In line with the notion that antibody response is higher in severe patients, a large population study (n = 30,576 persons from Iceland) (Gudbjartsson et al., 2020) conducted in Iceland revealed similar observation. The study provided a comprehensive account of the relation of antibody response concerning age, sex, body-mass index, drugs habits like smoking and the use of anti-inflammatory medication. Results show that patients with smoking habit and who were on anti-inflammatory medication, had lower antibody levels, while body mass index had a positive association. The data thus suggest that antibody response may not always favor clearance of the virus, but in some instances, higher antibody levels may make the patients more vulnerable to the disease.\nThis detrimental relation of antibody response with poor disease outcome was also prevalent in the previous SARS-CoV infection (Zhang et al., 2006). In a study on the sera samples obtained from SARS-CoV infected patients, a faster S protein-specific antibody response was found in patients who did not survive (14.7 days), as compared with the patients who recovered from the disease (20 days). Further, the antibody titer was significantly higher in the deceased patients with faster production than in the recovered patients. To mechanistically understand why antibody response has a more detrimental effect than protective, Liu et al. (2019) studied viral antibody response in animal models (Chinese rhesus monkeys). When animals infected with the SARS-CoV and adoptively transferred with anti-S protein IgG could not prevent the infection but instead displayed severe disease symptoms. Presence of the S protein antibody abrogated wound healing, induced macrophage/monocyte infiltration into the lungs and caused the release of proinflammatory cytokine followed by acute lung injury. This study thus demonstrated that the presence of S protein-specific antibody might have a deleterious effect in inducing lung injury, irrespective of the viral load. However, since mechanistic details are difficult to discern in clinical samples, more studies in animal models need to be explored. Further, owing to the dynamics of antibody response in clinical samples concerning underlying disease condition, age, and genetic factors; animal models will provide a cleaner system to delineate the antibody dynamics with respect to disease severity (Guan et al., 2020; Hou et al., 2020).\nContrary to B cell activation, some studies have shown lower antibody durability in both mild and severe cases (Yu et al., 2020). In a longitudinal study on a 26-year-old woman with a moderate disease condition, antibody response disappeared within three months (Liu A. et al., 2020). In a sizable cohort of samples, asymptomatic patients (n = 37 with median age 41 years) had relatively lower durability of the IgG and IgM antibodies in comparison to the symptomatic patients (n = 37). Further, the viral shedding in the asymptomatic group was higher than the symptomatic group (Long et al., 2020b). Similarly, Ibarrondo et al. has shown the same antibody durability in 34 COVID-19 patients with a mean age of 43 years when studied longitudinally for a period of upto 4 months (Ibarrondo et al., 2020). The authors found a significant decline in IgG antibodies in the sera of convalescent patients with mostly mild symptoms. A declining trend was seen for multiple SARS-CoV-2 antibodies like IgG N, IgM, IgG S1, and IgA S1 in the longitudinal analysis (n = 487) (Gudbjartsson et al., 2020). In another longitudinal study, the disappearance of S and N protein-specific antibodies was observed within 3 months of recovery (Liu A. et al., 2020). Based on these reports, we can infer that the antibody response in some COVID-19 patients may not be long-lasting, which poses a challenge for antibody-based therapy and vaccine research—further, these data caution towards chances of reinfection, as shown to be the case with other seasonal coronaviruses (Edridge et al., 2020). However, larger cohort size and longer time frame longitudinal studies are needed to find the durability of antibody response in COVID-19.\nFurther, a comparison of various disease states with corresponding antibody response will provide clearer insight as to how this response is regulated. It appears that in patients with severe disease symptoms, TNF-α may influence the GC and hence B cell number (Kaneko et al., 2020), whether the same holds for asymptomatic patients with compromised antibody durability remains elusive. This dynamic antibody response is critical while considering convalescent plasma therapy (CPT) for severe or critically ill patients. If a patient already has sufficient antibodies, CPT may not be a viable treatment option (Anderson et al., 2020; Duan et al., 2020). While many studies have reported success with CPT, some studies have shown no added beneficial effects with this approach (Li L. et al., 2020). Thus, pre-caution should be taken while using this approach, i.e., if a patient already has adequate virus-specific antibodies or presence of cross-reactive and auto-antibodies, plasma therapy may do more harm than good, which may be the reason with non-responsiveness of CPT in some patients (Nagoba et al., 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