Dataset Information

Severe Acute Respiratory Syndrome Coronavirus 2 Antibody Seroprevalence in Lebanon: A Population-Based Cross-Sectional Study

ABSTRACT:

Objectives

The World Health Organisation promoted the use of serological testing as a rapid and accurate technique for detection of the immunity against Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). In Lebanon, a better understanding of the immune response against SARS-CoV-2 is needed to develop effective measures for prevention and plan an appropriate national vaccination program. This study aims to measure the immunity status in Lebanon.

Methods

In this cross-sectional study, the population consisted of male and female Lebanese and non-Lebanese residents of Lebanon between the ages 15 and 75. Exclusion criteria included same household, symptomatic individuals, and extremes of age (<15 and >75). Representative testing for SARS-CoV-2 antibodies (Anti-SARS-CoV-2 electrochemiluminescence immunoassay/ECLIA) was used to assess the prevalence of SARS-CoV-2 infection in Lebanon.

Results

Over 6 months, a total of 13,755 participants were recruited, and 3,168 (23.03%) individuals tested positive for Anti-SARS-CoV-2, with levels of positivity varying among districts. A higher level of seropositivity was detected in the female participants.

Conclusion

The seroprevalence against SARS-CoV-2 varied within Lebanon and was compatible with the levels seen in the MENA region at the time of the study. The seroprevalence documented in this study reflected a level of immunity that is not protective at the national level.

Funding

This study was funded by the Lebanese American University School of Medicine.

SUBMITTER: Mahdi A

PROVIDER: S-EPMC8800496 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BACKGROUND: Public health risks associated to infection by human coronaviruses remain considerable and vaccination is a key option for preventing the resurgence of severe acute respiratory syndrome coronavirus (SARS-CoV). We have previously reported that antibodies elicited by a SARS-CoV vaccine candidate based on recombinant, full-length SARS-CoV Spike-protein trimers, trigger infection of immune cell lines. These observations prompted us to investigate the molecular mechanisms and responses to antibody-mediated infection in human macrophages. METHODS: We have used primary human immune cells to evaluate their susceptibility to infection by SARS-CoV in the presence of anti-Spike antibodies. Fluorescence microscopy and real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR) were utilized to assess occurrence and consequences of infection. To gain insight into the underlying molecular mechanism, we performed mutational analysis with a series of truncated and chimeric constructs of fragment crystallizable ? receptors (Fc?R), which bind antibody-coated pathogens. RESULTS: We show here that anti-Spike immune serum increased infection of human monocyte-derived macrophages by replication-competent SARS-CoV as well as Spike-pseudotyped lentiviral particles (SARS-CoVpp). Macrophages infected with SARS-CoV, however, did not support productive replication of the virus. Purified anti-viral IgGs, but not other soluble factor(s) from heat-inactivated mouse immune serum, were sufficient to enhance infection. Antibody-mediated infection was dependent on signaling-competent members of the human Fc?RII family, which were shown to confer susceptibility to otherwise naïve ST486 cells, as binding of immune complexes to cell surface Fc?RII was necessary but not sufficient to trigger antibody-dependent enhancement (ADE) of infection. Furthermore, only Fc?RII with intact cytoplasmic signaling domains were competent to sustain ADE of SARS-CoVpp infection, thus providing additional information on the role of downstream signaling by Fc?RII. CONCLUSIONS: These results demonstrate that human macrophages can be infected by SARS-CoV as a result of IgG-mediated ADE and indicate that this infection route requires signaling pathways activated downstream of binding to Fc?RII receptors.