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Variations in the TLR7 gene have been linked to impaired immune signaling, which may increase a person's risk of developing secondary infections and developing severe COVID-19. Objectives: To investigate the relationship between variations in the TLR7 gene and the prevalence of co-infections and secondary bacterial pneumonia among hospitalized COVID-19. Methods: A case-control study was a hospital-based study done among 200 RT-PCR-confirmed COVID-19 patients. The secondary bacterial pneumonia (SBP) was determined as another type of clinical deterioration that appeared over 48 hours of admission and was proven by radiological infiltrates and the increase of inflammatory factors; the microbiological confirmation was viewed as supportive but not obligatory. Hardy-Weinberg equilibrium of the female control group was checked, and the genotype was determined with the help of Taqman SNP assays. Results: The average age of the participants was 45.6 ± 12.3 years, and 60 percent of them were men. Among the SBP cases, 85% had microbiological confirmation, while 15% fulfilled predefined clinical, radiological, and inflammatory marker–based criteria for SBP despite negative cultures. Hence, pathogens in SBP cases were Klebsiella pneumoniae 25%, as well as Staphylococcus aureus 35%. Conclusions: TLR7 gene polymorphisms were substantially linked to a roughly three-fold higher risk of secondary bacterial pneumonia in this cohort of hospitalized COVID-19 adults, ages 18 to 65. These results imply that bacterial superinfection may be predisposed by compromised TLR7-mediated antiviral innate responses.