Correct option is D
Explanation:
Statement A: Flagellin mutation in Proteobacteria prevents recognition by TLRs - Correct
Flagellin is the structural protein of bacterial flagella.
It is recognized by TLR5, a pattern recognition receptor on host immune cells, triggering innate immune responses.Immune Evasion:
Some Proteobacteria have evolved mutations in flagellin that reduce or prevent its recognition by TLR5.
This allows them to avoid activating innate immunity, helping in immune evasion and persistence.
Statement B: LPS mutations in Helicobacter prevent TLR recognition- Correct
Lipopolysaccharide (LPS) is a key component of the outer membrane of Gram-negative bacteria and is recognized by TLR4.
Immune Evasion:
Helicobacter pylori modifies its LPS structure (e.g., altered lipid A) to reduce TLR4 recognition.
This dampens immune activation and allows it to persist in the harsh gastric environment.
Statement C: M. tuberculosis escapes phagosome to cytosol -Incorrect
M. tuberculosis is an intracellular pathogen that infects macrophages.
Immune Evasion:
Instead of escaping to the cytosol, M. tuberculosisprevents phagosome-lysosome fusion, allowing it to survive inside the phagosome.
Cytosolic escape is more typical of bacteria like Listeria monocytogenes.
Statement D: Influenza virus produces Yop protein - Incorrect
Yop proteins are secreted by Yersinia species via Type III secretion system to inhibit inflammasomes and immune signaling.
Influenza Virus:
Influenza virus does not produce Yop proteins. It uses other mechanisms (e.g., NS1 protein) to evade immune responses.
Statement E: S. typhi protein binds Type I IFNs - Incorrect
Salmonella typhi evades host immunity through multiple mechanisms, including interference with cytokine signaling.
Protein binding Type I IFNs:
While S. typhi modulates immune signaling, specific binding of Type I IFNs to prevent receptor binding is not a well-characterized or widely accepted mechanism for this pathogen.
