Hepatitis MCQs

Ans. is 'c' i.e., Plaque assay Plaque assay and Pock assay are quantitative infective assays.

Glomerulonephritis is often associated with immune complex deposition, a type III hypersensitivity. Red blood cell casts are indicative of glomerulonephritis, and reduced C3 levels indicate a high level of cleavage and activation of C3. Type I hypersensitivity is mediated by IgE, not by CD4+ T cells. Type II hypersensitivity responses usually involve IgG. Type IV hypersensitivities do not involve antibodies. Reference: Ananthanarayan and Paniker's Textbook of Microbiology 10th edition Chapter 16, Pg 164-168

Hepatitis B serologies can reveal significant information about the status of hepatitis B in any given patient. Major components of the test include HBsAg (surface antigen), HBsAb (surface antibody), HBc IgM (core IgM antibody), and HBc IgG (core IgG antibody). Immunization from a previous infection indicates previous exposure to viral antigens and subsequent development of antibodies against both to the surface and core antigens. Patients who develop antibodies against the viral envelope antigen (HBeAb) are more likely to achieve long-term clearance of the virus. Reference: Essentials of Medical Microbiology, by Apurba Sastry and Sandhya Bhat, 3rd Edition, Page 487

Hepatitis B core antigen, or HBcAg is an intracellular core protein, hence it is not secreted in blood. However, it can be demonstrated in hepatocytes by immunofluorescence. HBeAg is a non-particulate soluble antigen and is present in circulation. HBsAg, also called Australia antigen is the first to be elevated following an infection. Anti HBC IgM is the first antibody to be elevated following an infection. Reference: Essentials of Medical Microbiology, byApurba Sastry and Sandhya Bhat, 3rd edition, page 479

This case describes escape mutation seen in the HBV genome. The escape mutants of HBV have mutations in the S gene which leads to alteration of HBsAg. Escape mutants are observed in three situations: Infants born to HBeAg positive mothers liver transplant recipients who underwent the procedure for hepatitis B and who were treated with a high-potency human monoclonal anti-HBs preparation A small proportion of recipients of active and passive immunization, in whom antibody pressure may favor evolutionary change in gene coding an antigen. Patients infected with escape mutants lack HBsAg and therefore are often underdiagnosed by routine serological test for HBsAg Reference: Essentials of Medical Microbiology, by Apurba Sastry and Sandhya Bhat, 3rd edition, page 480

PAN is a small/medium vessel vasculitis. It follows HBV/HCV infection. It is characterized by the presence of inflammatory reactions of medium or small-sized blood vessels with multiorgan involvement including skin, kidney, peripheral nerve, muscle, gastrointestinal tract and others. Reference : Bailey and Love's Short Practice of Surgery, 28th Edition, Chapter: 17, Pg: 268

This patient's scleral icterus and jaundice should raise suspicion for liver disease. His pruritic rash that worsens upon exposure to sunlight is suggestive of Porphyria Cutanea Tarda (PCT), a condition that is associated with hepatitis C virus infection. Reference: Essentials of Medical Microbiology, by Apurba Sastry and Sandhya Bhat, 3rd Edition, Page 487

HBsAg is also known as Australia antigen. It is the first to be elevated following an infection. HBsAg is a protein on the surface of HBV. Continuous presence of HBsAg indicates carrier state. Without HBsAg, Anti-HBs indicates immunity to HBV due to resolved infection or vaccination. Usually appears ∼ 1-3 months after infection or vaccination. Reference: Essentials of Medical Microbiology, by Apurba Sastry and Sandhya Bhat, 3rd Edition, Page 487