Background The inactivated Sinopharm/BBIBP COVID‐19 vaccine has been widely used in the world and has joined the COVAX vaccine supply program for developing countries. It is also well adapted for usage in low‐ and middle‐income nations due to their low storage requirements. Objective This study aims to report on the kinetics, durability, and neutralizing ability of the induced immunity of the BBIBP vaccine, and the intensified antibody response elicited by the booster. Methods A total of 353 healthy adult participants, aged 20–74 years, were recruited in this multicenter study. A standard dose of the BBIBP vaccine was administered (Month 0), followed by a second standard dose (Month 1), and a booster dose (after Month 7). Vaccine‐induced virus‐specific antibody levels (SARS‐CoV‐2‐IgA/IgM/IgG), conventional virus neutralization test (cVNT), pseudovirus neutralization test (pVNT), and surrogate virus neutralization test (sVNT) were monitored over multiple time points. Results Neutralizing titers induced by the two doses of inactivated vaccine for COVID‐19 peaked at Month 2 and declined to 33.89% at Month 6. Following the booster dose, elevated levels of antibodies were induced for IgA, IgG, and neutralizing antibodies, with neutralizing titer reaching 13.2 times that of before the booster. Conclusion By monitoring the antibody titer levels postvaccination, this study has shown that serum antibody levels will decrease over time, but a notable spike in antibody levels postbooster highlights the anamnestic immune response. This signifies that the protection capability has increased following the injection of booster immunization.

The newly identified Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has resulted in a global health emergency (COVID-19) because of its rapid spread and high mortality. Since the virus epidemic, many pathogenic mechanisms have been revealed, and virus-related vaccines have been successfully developed and applied in clinical practice. However, the pandemic is still developing, and new mutations are still emerging. Virus pathogenicity is closely related to the immune status of the host. As innate immunity is the body’s first defense against viruses, understanding the inhibitory effect of SARS-CoV-2 on innate immunity is of great significance for determining the target of antiviral intervention. This review summarizes the molecular mechanism by which SARS-CoV-2 escapes the host immune system, including suppressing innate immune production and blocking adaptive immune priming. Here, on the one hand, we devoted ourselves to summarizing the combined action of innate immune cells, cytokines, and chemokines to fine-tune the outcome of SARS-CoV-2 infection and the related immunopathogenesis. On the other hand, we focused on the effects of the SARS-CoV-2 on innate immunity, including enhancing viral adhesion, increasing the rate of virus invasion, inhibiting the transcription and translation of immune-related mRNA, increasing cellular mRNA degradation, and inhibiting protein transmembrane transport. This review on the underlying mechanism should provide theoretical support for developing future molecular targeted drugs against SARS-CoV-2. Nevertheless, SARS-CoV-2 is a completely new virus, and people’s understanding of it is in the process of rapid growth, and various new studies are also being carried out. Although we strive to make our review as inclusive as possible, there may still be incompleteness.

Serial chest computed tomography scans of four patients since symptom onset. (1) Patient A: (A and D) diffuse bilateral groundglass opacities (GGOs) predominantly involving perihilar and midzones with relative subpleural sparing at 3 weeks after symptom onset. (B and E) A mixed pattern of GGOs, reticulation and air space consolidation, cystic airspaces, decreased lung volume, and compensatory increased anteriorposterior chest diameter at 9 weeks. (C and F) Partial resolution of various lesions at 12 weeks. (2) Patient B: (A and D) diffuse irregular GGOs mainly with subpleural and peripheral involvement 10 days after symptom onset. (B and E) Confluence of peripheral lesions in the left upper lung and a mixed pattern of ground-glass and reticular opacities in the lower lung bilaterally at six weeks. (C and F) Lesion resolution with some remnant GGOs at 8 weeks. (3) Patient C: (A) irregular GGOs at the periphery of the lower lung bilaterally 4 weeks after symptom onset. (B) Enlarged areas of GGOs bilaterally and an irregular nodule in the right lower lung at 6 weeks. (C) minimal residual opaque lesions at eight weeks. (4) Patient D: (A) wedge-shaped GGOs at the periphery of the right upper lung and the left upper lung medially 2 days after symptom onset. (B) Enlarging area of GGOs bilaterally with reticulation and consolidation in the left lung at three weeks. (C) Partial resolution of GGOs at 5 weeks