Host Defence and Pathogenesis

Macrophages are the first line of defence against M. tuberculosis. The lab examines how these cells detect and respond to infection, including:

• Activation of antimicrobial pathways
• Regulation of phagosome maturation and acidification
• Host mechanisms that restrict bacterial survival

This work defines how effective immune responses are initiated and sustained.

The lab studies how M. tuberculosis disrupts host immune function to persist داخل cells. This includes:

• Bacterial factors that block antimicrobial activity
• Interference with intracellular trafficking pathways
• Disruption of host immune signaling

These mechanisms allow the pathogen to survive and replicate within host cells.

The research explores how signaling pathways shape infection outcomes in both the host and pathogen. Areas of focus include:

• Mycobacterial kinases and phosphatases that regulate virulence
• Host signaling pathways targeted during infection
• Molecular communication between pathogen and host

This work shows how signaling controls both immune responses and bacterial adaptation.

The Av-Gay Lab identified PtpA as a key virulence factor in M. tuberculosis.

• PtpA is secreted into host cells during infection
• It interferes with host trafficking processes
• It blocks phagosome acidification, reducing bacterial clearance

This provides a clear example of how bacterial proteins directly disrupt host defence systems.

The lab connects insights from pathogenesis to treatment development. This includes:

• Identifying targets in bacterial survival pathways
• Developing host-directed therapies
• Exploring strategies to restore immune function

This work supports new approaches to treating persistent infection.