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To do so, we search for stable stationary or periodic solutions of this model with low viral load that can be interpreted as long COVID using our recently developed technology for analysing time-delay systems. The results of the bifurcation and sensitivity analysis of the mathematical model of SARS-CoV-2 infection suggest the following biological conclusions concerning the mechanisms of pathogenesis of long COVID-19. First, the possibility of SARS-CoV-2 persistence requires a 3-time reduction of the virus production rate per infected cell, or 18-times increase of the antibody-mediated elimination rate of free viruses as compared to an acute infection baseline estimates. Second, the loss of kinetic coordination between virus-induced type I IFN, antibody, and cytotoxic T lymphocyte (CTL) responses can result in the development of mild severity long-lasting infection. Third, the low-level persistent SARS-CoV-2 infection is robust to up to 100-fold perturbations (increase) in viral load and most sensitive to parameters of the humoral immune response. <\/jats:p>","DOI":"10.1142\/s0219720025400013","type":"journal-article","created":{"date-parts":[[2025,1,24]],"date-time":"2025-01-24T10:01:13Z","timestamp":1737712873000},"source":"Crossref","is-referenced-by-count":1,"title":["Computation and analysis of stationary and periodic solutions of the COVID-19 infection dynamics model"],"prefix":"10.1142","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0391-7319","authenticated-orcid":false,"given":"Michael","family":"Khristichenko","sequence":"first","affiliation":[{"name":"Marchuk Institute of Numerical Mathematics, Russian Academy of Sciences, Moscow 119333, 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