Q10. Explain how a defect in CD40L leads to the Hyper-IgM phenotype. (2-3 sentences) (2 marks)

Q13. Doctors suspect that the causative bacterium is part of Terry’s normal skin microbiota that entered the body via a small cut on his knee, leading to abscess formation. How would you classify this infection? (select all that apply)

Q15. The causative bacterium secretes a toxin which forms pores in host cell membranes and causes cell lysis. Secretion of this toxin contributes to the tissue damage observed in Terry’s abscess. How would you classify this toxin?

Q11. How will an excess of IgM (but a lack of IgG and IgA) affect Terry’s humoral immune response to extracellular bacteria? (2-3 sentences) (2 marks)

Q17. The doctor initiates antibiotic therapy with polymyxin while awaiting antibiotic susceptibility testing results for the causative bacterium. Explain why polymyxin is not a suitable antibiotic therapy in this situation. (2-3 sentences) (2 marks)

Q16. The causative bacterium also secretes hyaluronidase. Explain how this enzyme likely contributes to bacterial pathogenesis and the formation of abscesses. (1-2 sentences) (2 marks)

Q12. Is Terry’s inflammatory response likely intact or impaired by his immunodeficiency? Use the information provided in this case study to justify your response. (2-3 sentences) (2 marks)

Q5. RhoV has been associated with increased rates of lung carcinoma in individuals with long-term infection. Explain how RhoV infection could contribute to oncogenesis. (2-3 sentences) (2 marks)

Q8. What type of antibody response would you aim to elicit through vaccination, and how would this response protect against RhoV? (2-3 sentences) (2 marks)

Q4. After the initial period of respiratory illness, the virus enters a dormant phase within host cells and may reactivate months or years later when immunity wanes. Which term would you use to describe RhoV infection during this dormant phase?