Govt. Exams
Entrance Exams
The N501Y mutation (asparagine to tyrosine at position 501) in the receptor binding domain (RBD) of the spike protein significantly increased the binding affinity to human ACE2 receptors in the Alpha variant. This mutation altered the molecular interactions at the RBD-ACE2 interface, enhancing viral attachment and contributing to the variant's higher transmissibility observed during 2020-2021.
Biofilm-mediated persistence involves multiple factors: slow growth reduces drug efficacy, polysaccharide matrix blocks penetration, and phenotypic variants (persisters) survive treatment.
CD8+ cytotoxic T lymphocytes produce IFN-γ upon encountering virus-infected cells presenting viral antigens on MHC-I, indicating cellular immune response activation.
N. gonorrhoeae uses gene conversion to shuffle silent pili gene segments, creating new surface antigens faster than immune response, enabling chronic infection.
3CL^pro is highly conserved, essential for viral maturation, and structurally distinct from human enzymes, making it an excellent target for antivirals like nirmatrelvir.
Restriction-modification systems use restriction endonucleases to cut foreign DNA at specific recognition sites while protecting host DNA through methylation.
Increased spike protein affinity would enhance binding to ACE2 receptors, improving viral attachment and entry efficiency, particularly relevant to emerging variants.
Recent variants like XEC demonstrate accumulated mutations in the receptor binding domain conferring immune escape properties.
Mycobacterium tuberculosis inhibits phagolysosome maturation and produces catalase to neutralize reactive oxygen species.
Type I interferons (IFN-α/β) are crucial for antiviral immunity; defects impair early viral containment.
