Question 1

Hepatocellular carcinoma (hepatoma) aetiology: Which hepatitis viruses are established risk factors for primary liver cancer?

Accepted Answer

Introduction: Hepatocellular carcinoma (HCC) arises in the setting of chronic liver disease and cirrhosis. Viral hepatitis is a major global driver. The two hepatitis viruses consistently implicated as causal risk factors are HBV and HCV. Given Data / Assumptions: We must identify which hepatitis viruses are established causes of HCC. Chronicity and oncogenic mechanisms differ between hepatitis viruses. HAV does not cause chronic infection and is not a recognized cause of HCC. Concept / Approach: HBV is oncogenic via chronic necroinflammation, integration of HBV DNA into the host genome, and expression of HBx protein that affects cell cycle and apoptosis. HCV promotes HCC primarily via chronic inflammation, fibrosis, cirrhosis, and indirect oncogenic signaling; it is an RNA virus and does not integrate like HBV. Both infections are major HCC risk factors worldwide. Step-by-Step Solution: Exclude HAV, which causes acute, self-limited hepatitis without chronic carriage. Recognize HBV as a direct and indirect oncogenic virus. Recognize HCV as an indirect oncogenic virus via chronic hepatitis and cirrhosis. Select the combined option covering HBV and HCV. Verification / Alternative check: Epidemiologic data show high HCC incidences in regions endemic for HBV or with significant HCV burden; antiviral control reduces HCC risk, supporting causality. Why Other Options Are Wrong: HBV only / HCV only: Each is incomplete because both are established causes. HAV / None of these: HAV is not linked to HCC due to lack of chronicity. Common Pitfalls: Assuming all hepatitis viruses behave similarly; chronicity is the key determinant for carcinogenic risk. Final Answer: Both HBV and HCV are established causes of HCC.

Question 2

Hepatitis B virus (HBV) genome type: Which nucleic acid form characterizes HBV?

Accepted Answer

Introduction: HBV is the prototype of the Hepadnaviridae family, notable for its unusual genomic organization and reverse transcription step. Identifying its nucleic acid type is a fundamental virology fact. Given Data / Assumptions: HBV virions contain a relaxed circular DNA genome with one complete and one incomplete strand. The replication cycle includes reverse transcription of an RNA intermediate inside nucleocapsids. We must choose the best descriptor of the incoming genome in virions. Concept / Approach: HBV packages a partially double-stranded DNA molecule. After infection, host repair completes the gap to form covalently closed circular DNA (cccDNA) in the nucleus. Although reverse transcription occurs during replication, the genome present in virions is DNA, not RNA. Step-by-Step Solution: Recall that HBV is a DNA virus with reverse transcription. Identify the virion genome as relaxed circular partially dsDNA. Select the option that explicitly states partially dsDNA for maximum precision. Verification / Alternative check: Electron microscopy and biochemical analyses confirm the gapped DNA structure, later repaired to cccDNA intracellularly. Why Other Options Are Wrong: ssRNA / dsRNA / negative-sense RNA: Do not describe HBV; those apply to RNA virus families. ssDNA: Not the HBV genome state in virions. Common Pitfalls: Confusing the use of reverse transcriptase with being an RNA virus; HBV is a DNA virus with a unique replication strategy. Final Answer: HBV contains partially double-stranded DNA in virions.

Question 3

Enveloped hepatitis viruses: All of the following are enveloped except which virus?

Accepted Answer

Introduction: The presence or absence of a lipid envelope influences environmental stability, transmission route, and resistance to disinfectants. Among hepatotropic viruses, envelope status is a high-yield identification point. Given Data / Assumptions: We must pick the non-enveloped virus among listed hepatitis viruses. HAV and HEV typically spread fecal–oral; HBV, HCV, and HDV spread mainly via blood and body fluids. Concept / Approach: HAV is a non-enveloped, positive-sense RNA virus in the Picornaviridae family (genus Hepatovirus), conferring environmental resilience. HBV (Hepadnaviridae), HCV (Flaviviridae), and HDV (a defective RNA agent requiring HBV) are enveloped. HEV is non-enveloped in stool but can be quasi-enveloped in blood; however, the classic exam contrast focuses on HAV as the archetypal non-enveloped member among the choices. Step-by-Step Solution: List envelope status for each hepatitis virus. Identify HAV as classically non-enveloped and environmentally hardy. Select HAV as the exception among enveloped viruses. Verification / Alternative check: Textbook virology differentiates enteric non-enveloped HAV from blood-borne enveloped HBV, HCV, and HDV. Why Other Options Are Wrong: HBV / HCV / HDV: Enveloped viruses transmitted parenterally and via body fluids. HEV: Often considered non-enveloped in stool; some curricula may not include it in the classic list; the most consistent single best answer here is HAV. Common Pitfalls: Overlooking special quasi-envelope forms of HEV in blood; for standard MCQ framing, HAV is the clear non-enveloped pick. Final Answer: Hepatitis A virus (HAV) is not enveloped.

Question 4

Hepatitis viruses transmitted by parenteral and sexual routes: Which of the following fit this mode of transmission?

Accepted Answer

Introduction: Transmission routes determine screening policies, prevention strategies, and counseling. Several blood-borne hepatitis or hepatitis-associated viruses spread via parenteral exposures and, to varying degrees, sexual contact. Given Data / Assumptions: HBV, HCV, and Hepatitis G virus (GBV-C) are listed. Parenteral includes transfusion, needle sharing, occupational exposures. Sexual transmission efficiency differs among viruses. Concept / Approach: HBV is efficiently transmitted by both parenteral and sexual routes. HCV is primarily parenteral; sexual transmission is less efficient but documented, especially with high-risk exposures. GBV-C (Hepatitis G virus) is parenterally transmitted and has been detected in sexually transmitted contexts. Therefore, all listed agents can follow these routes. Step-by-Step Solution: Confirm parenteral spread for HBV, HCV, and GBV-C. Acknowledge sexual transmission: high for HBV, lower yet present for HCV and GBV-C. Select the inclusive option since all listed viruses qualify. Verification / Alternative check: Serologic and epidemiologic studies support these routes, with prevention relying on safe injections, blood screening, barrier protection, and HBV vaccination. Why Other Options Are Wrong: Any single virus alone: Incomplete because multiple viruses listed fit the criteria. None of these: False based on extensive transmission evidence. Common Pitfalls: Assuming HCV has no sexual transmission; although less efficient, it can occur, particularly with co-factors like high viral load or mucosal injury. Final Answer: All of these viruses have parenteral and sexual transmission routes.

Question 5

Taxonomy of Hepatitis G virus (GB virus C): To which virus family does it belong?

Accepted Answer

Introduction: Hepatitis G virus, more accurately known as GB virus C, is not a classic hepatitis virus causing liver disease, yet it clusters phylogenetically with a familiar RNA virus family. Correct classification aids understanding of genome organization and replication. Given Data / Assumptions: We must assign Hepatitis G virus (GBV-C) to the correct family. Genome type and polyprotein strategy suggest a specific family. Concept / Approach: GBV-C is a positive-sense single-stranded RNA virus grouped within Flaviviridae, historically alongside HCV. It shares the general flaviviral genomic layout: a single ORF translated into a polyprotein processed into structural and nonstructural proteins. Step-by-Step Solution: Recall that HCV and GBV-C are positive-sense RNA viruses with similar replication strategies. Map this to the Flaviviridae family. Select Flaviviridae as the correct classification. Verification / Alternative check: Molecular phylogeny and genome organization studies consistently place GBV-C within Flaviviridae. Why Other Options Are Wrong: Caliciviridae / Coronaviridae / Paramyxoviridae: Different genome organizations and replication strategies. Hepadnaviridae: DNA viruses with reverse transcription, unlike GBV-C RNA genome. Common Pitfalls: Assuming the name “Hepatitis G” implies similar biology to HBV; naming is historical and does not reflect family membership. Final Answer: Hepatitis G virus belongs to Flaviviridae.

Question 6

Parenteral transmission: Which of the following hepatitis viruses can be transmitted by parenteral exposure?

Accepted Answer

Introduction: Parenteral transmission includes transfusion, needle sharing, and percutaneous exposures. Several hepatitis viruses spread efficiently by these routes, with implications for screening and infection control. Given Data / Assumptions: The listed viruses are HBV, HCV, and HDV. We seek which are transmissible through parenteral exposure. Concept / Approach: HBV and HCV are archetypal blood-borne pathogens. HDV is a defective RNA virus that requires HBV for replication; its spread mirrors HBV, including parenteral exposure. Therefore all listed viruses can be parenterally transmitted. Step-by-Step Solution: Confirm HBV and HCV parenteral routes (widely documented). Recognize HDV co-transmission with HBV through the same exposures. Choose the inclusive option that captures all three. Verification / Alternative check: Blood bank screening, harm reduction, and vaccination strategies target these agents specifically due to parenteral risk. Why Other Options Are Wrong: Any single-virus option: Incomplete; all three are parenterally transmissible. None of these: Contradicted by extensive epidemiology. Common Pitfalls: Overlooking HDV because it is dependent on HBV; dependence does not negate its parenteral spread when HBV is present. Final Answer: All of these are transmitted by parenteral routes.

Question 7

Diagnosis of acute hepatitis E: Which laboratory test is the most reliable for detecting recent HEV infection?

Accepted Answer

Introduction: Hepatitis E typically presents as an acute, self-limited hepatitis with fecal–oral transmission. Accurate laboratory diagnosis focuses on detecting markers of recent infection, especially in outbreak settings and in pregnant patients where disease can be severe. Given Data / Assumptions: The aim is to detect recent or ongoing HEV infection. Available assays include serology (IgM, IgG) and nucleic acid testing (PCR). We consider reliability and practicality for routine diagnosis. Concept / Approach: IgM anti-HEV appears during acute infection and is widely used for diagnosis via ELISA. PCR for HEV RNA is highly specific and useful, especially early or in immunocompromised hosts, but may be less accessible and time dependent due to transient viremia and assay availability. Many clinical algorithms consider IgM ELISA the most reliable front-line test for acute HEV in routine practice. Step-by-Step Solution: Define the clinical target: recent infection. Match serologic marker: IgM positivity indicates acute phase. Select ELISA for IgM anti-HEV as the standard, reliable, and widely used test. Verification / Alternative check: Public health guidance and common lab workflows endorse IgM ELISA as first-line in outbreaks; PCR complements serology when necessary. Why Other Options Are Wrong: Western blot IgM: Confirmatory, not routine front-line, and less widely available. PCR HEV RNA: Very specific but limited by availability and timing; not always the chosen routine single best answer. ELISA IgG: Indicates past exposure rather than recent infection. Rapid antigen: Not standard for definitive acute HEV diagnosis. Common Pitfalls: Assuming PCR always equals most reliable; in many settings, validated IgM ELISA provides the best combination of sensitivity, specificity, and feasibility. Final Answer: ELISA for IgM anti-HEV is the most reliable routine test for acute HEV.

Question 8

Vertical transmission risk: Which hepatitis viruses among the following are known to have mother-to-child (perinatal) transmission?

Accepted Answer

Introduction: Vertical transmission affects neonatal outcomes and prevention strategies such as maternal screening, antiviral therapy, and immunoprophylaxis. Multiple hepatitis viruses can be transmitted perinatally under specific conditions. Given Data / Assumptions: We consider perinatal transmission rates and mechanisms. HBV, HCV, and HDV are listed. HDV requires HBV for transmission and replication. Concept / Approach: HBV has significant perinatal transmission risk, especially with high maternal viral load and HBeAg positivity; immunoprophylaxis at birth is crucial. HCV vertical transmission occurs, with risk factors including high maternal viremia and HIV coinfection. HDV may be vertically transmitted when HBV is present, though efficiency varies by epidemiology. Step-by-Step Solution: Acknowledge strong perinatal risk for HBV and its prevention with HBIG plus vaccine. Recognize documented though lower-rate vertical transmission for HCV. Include HDV in contexts of maternal HBV coinfection. Choose the inclusive option covering all three viruses. Verification / Alternative check: Clinical guidelines address perinatal HBV prophylaxis; studies confirm measurable vertical HCV transmission; HDV follows HBV epidemiology. Why Other Options Are Wrong: HBV / HCV alone: Incomplete; HDV can also be transmitted in HBV coinfection settings. None of these: Contradicted by established perinatal transmission data. Common Pitfalls: Assuming HDV cannot be vertically transmitted; while less frequent, it is possible when HBV is present. Final Answer: All of these can be transmitted vertically under the appropriate conditions.

Question 9

Defective satellite viruses in hepatitis – Identify the agent that requires hepatitis B virus (HBV) for its replication and assembly (envelope supply).

Accepted Answer

Introduction: Among the human hepatitis viruses, one agent is unique because it cannot complete its life cycle without help from another virus. This question tests your understanding of the defective satellite nature of hepatitis D virus (HDV) and why it depends on hepatitis B virus (HBV) for infectious particle formation. Given Data / Assumptions: HDV possesses a circular single-stranded RNA genome and delta antigen (HDAg). HBV provides the envelope protein (HBsAg) needed for HDV virion assembly and egress. HDV can infect as coinfection with HBV or as superinfection in an existing HBV carrier. Concept / Approach: Classify hepatitis viruses by structure and replication requirements. Identify which agent is a satellite virus: one that uses another virus's proteins to package its genome and exit cells. Determine which hepatitis virus supplies the missing structural components for HDV. Step-by-Step Solution: Step 1: Recall that HDV lacks its own envelope glycoproteins and requires HBsAg from HBV.Step 2: Recognize that without concurrent HBV infection, HDV cannot assemble infectious virions.Step 3: Distinguish HDV from HAV, HCV, and HEV, which are independent viruses with their own assembly machinery.Step 4: Conclude that the defective satellite virus among the options is HDV. Verification / Alternative check: Clinical patterns support this biology: HDV coinfection causes acute hepatitis with HBV, while HDV superinfection of an HBsAg carrier often leads to severe disease because HBV supplies abundant HBsAg for HDV packaging. Why Other Options Are Wrong: HBV: a complete DNA virus; not defective. HCV: an RNA flavivirus; independent replication. HAV/HEV: enterically transmitted RNA viruses; no dependency on HBV. Common Pitfalls: Assuming all hepatitis viruses behave similarly; overlooking the requirement for HBsAg in HDV assembly. Final Answer: Hepatitis D virus (HDV).

Question 10

HBV serotypes in India – Identify the prevalent antigenic type of hepatitis B virus documented in the Indian subcontinent.

Accepted Answer

Introduction: Hepatitis B virus (HBV) exhibits antigenic variability in its surface antigen (HBsAg), producing serotypes such as adw, adr, ayw, and ayr. Recognizing regional prevalence patterns helps in epidemiology, vaccine evaluation, and interpreting sero-surveys. This question asks which serotype is prevalent in India. Given Data / Assumptions: HBsAg serotypes are defined by epitopes d/y and w/r on the surface antigen, combined with subtype determinants. India has historically shown predominance of the ayw serotype, with geographic variability. The question seeks the prevalent type, not an exclusive type. Concept / Approach: Recall classic epidemiologic mapping of HBV serotypes: ayw is common in the Middle East, Mediterranean, and Indian subcontinent; adw is prevalent in the Americas and parts of Europe; adr is notable in East Asia. Therefore, align India with ayw predominance. Step-by-Step Solution: Step 1: List canonical HBV serotypes and their geographic associations.Step 2: Match India with the ayw cluster from standard references.Step 3: Exclude adr (East Asia) and adw (Americas/Europe) as predominant Indian types.Step 4: Select ayw as the prevalent Indian serotype. Verification / Alternative check: Serologic studies and public health texts consistently report ayw predominance in India, though local pockets may show other types due to migration and viral evolution. Why Other Options Are Wrong: Adw/Adr/Ayr: documented elsewhere as common types but not predominant in India. Adu: not a standard HBV serotype in typical teaching sets. Common Pitfalls: Confusing genotype distributions (A–J) with serotype patterns (adw, ayw, etc.); assuming one serotype is globally dominant. Final Answer: Ayw.

Question 11

Laboratory diagnosis of acute hepatitis A – Choose the most appropriate method for confirming recent HAV infection.

Accepted Answer

Introduction: Accurate diagnosis of acute hepatitis A virus (HAV) infection is essential for clinical management and public health responses. While liver enzymes reflect hepatocellular injury, serologic tests identify etiology. This question evaluates your ability to select the standard confirmatory test for acute HAV infection. Given Data / Assumptions: Acute HAV typically presents with abrupt hepatitis and cholestatic features. Serology for anti-HAV IgM is the routine marker of recent infection. Advanced methods (e.g., immunoelectron microscopy, PCR) are not standard for routine diagnosis. Concept / Approach: Differentiate between nonspecific markers of liver injury (AST/ALT) and pathogen-specific assays. Identify which test is widely used, rapid, and reliable to confirm recent HAV: anti-HAV IgM by ELISA, which appears early and declines over months, distinguishing it from anti-HAV IgG indicating past exposure or vaccination. Step-by-Step Solution: Step 1: Recognize that elevated AST/ALT only indicate hepatitis, not its cause.Step 2: Note that immunoelectron microscopy is research-level and impractical for routine clinical labs.Step 3: Identify anti-HAV IgM ELISA as the standard confirmatory test for acute infection.Step 4: Consider that PCR is useful in specialized contexts but is not the frontline confirmatory tool in many settings. Verification / Alternative check: Guidelines and textbooks endorse anti-HAV IgM as the primary diagnostic marker for recent HAV, with anti-HAV IgG reflecting immunity from past infection or vaccination. Why Other Options Are Wrong: AST/ALT alone: nonspecific for etiology. Immunoelectron microscopy: not routine; low practicality. Both (a) and (b): still lacks a standard serologic confirmation. PCR only during convalescence: timing and availability issues; not standard first-line confirmation. Common Pitfalls: Equating biochemical hepatitis with a specific viral diagnosis; overlooking the diagnostic window and interpretation of IgM vs IgG. Final Answer: Detection of anti-HAV IgM by ELISA.

Question 12

Hepatitis G / GB viruses – Identify the isolate corresponding to the hepatitis G virus lineage.

Accepted Answer

Introduction: The term “hepatitis G virus” historically referred to viruses within the GB virus group discovered in studies of non-A–E hepatitis. Clarifying the nomenclature among GBV-A, GBV-B, and GBV-C helps avoid confusion in older literature and exam questions. This item asks which isolate corresponds to hepatitis G virus. Given Data / Assumptions: GB viruses are Flaviviridae-related RNA viruses identified in the 1990s. Hepatitis G virus is most closely associated with GBV-C in humans. Other GB viruses have different host ranges or experimental relevance. Concept / Approach: Map historical naming: GBV-C is the human virus often labeled hepatitis G virus. GBV-B is an experimental primate virus. GBV-A designations pertain to nonhuman primates. Therefore, select GBV-C when asked to identify the agent representing hepatitis G virus in people. Step-by-Step Solution: Step 1: List GB viruses and their typical hosts/associations.Step 2: Link hepatitis G nomenclature to GBV-C specifically.Step 3: Exclude nonhuman primate–restricted or experimental isolates for a human-associated label.Step 4: Choose GBV-C as the correct answer. Verification / Alternative check: Subsequent research often refers to GBV-C as human pegivirus (HPgV). Despite evolving taxonomy, exam contexts still equate hepatitis G virus with GBV-C. Why Other Options Are Wrong: GBV-B: primarily experimental hepatotropic virus in primates. GBA-A: not a standard designation in human hepatitis taxonomy. None of these/GBV-D: do not match the classic hepatitis G identification. Common Pitfalls: Assuming all GBVs infect humans equivalently; overlooking nomenclature updates to “pegivirus.” Final Answer: GBV-C (a.k.a. hepatitis G virus).

Question 13

Hepatitis G virus (GBV-C/HPgV) – Transmission routes: Identify the correct mode(s) of transmission documented for this agent.

Accepted Answer

Introduction: Hepatitis G virus, now often termed GBV-C or human pegivirus (HPgV), is detected in blood donors, persons with parenteral exposures, and some sexually exposed populations. This question checks recognition of the principal transmission routes implicated for this virus. Given Data / Assumptions: HPgV/GBV-C is found in the bloodstream and can be transmitted via contaminated needles or transfusion. Sexual transmission has been documented. There is no strong evidence of purely fecal–oral transmission analogous to HAV. Concept / Approach: Align epidemiologic patterns with transmission modes. Bloodborne and sexual routes mirror those of HBV/HCV to varying extents. Therefore, when options list parenteral and sexual routes, selecting both is appropriate. Step-by-Step Solution: Step 1: Associate detection in blood donors and IV drug users with parenteral spread.Step 2: Review studies indicating sexual transmission.Step 3: Exclude exclusive fecal–oral spread given limited supportive evidence.Step 4: Select “Both (a) and (b).” Verification / Alternative check: Seroprevalence studies and transfusion-screening data support bloodborne spread; cohort data support sexual transmission components. Why Other Options Are Wrong: Parenteral only or sexual only: incomplete. None of these: contradicted by epidemiologic evidence. Fecal–oral only: not the principal route for HPgV. Common Pitfalls: Assuming “hepatitis” always implies fecal–oral spread; conflating HAV/HEV with bloodborne agents. Final Answer: Both (a) and (b).

Question 14

Chronic carrier state in viral hepatitis – Identify which listed infections can result in chronicity and persistent carriage.

Accepted Answer

Introduction: Chronic hepatitis and carrier states drive cirrhosis and hepatocellular carcinoma risk and inform screening, vaccination, and therapy. This question asks which listed infections can result in chronic carriage. Given Data / Assumptions: HBV can persist, especially when acquired perinatally or in early childhood. HCV frequently becomes chronic in adults without spontaneous clearance. HDV requires HBV; chronicity can occur in HBV carriers who become superinfected with HDV. Concept / Approach: Evaluate each virus for documented chronic infection. HBV and HCV are well-known chronic infections. HDV superinfection in HBsAg carriers can also lead to chronic disease because HBV supplies the envelope, enabling ongoing HDV replication. Step-by-Step Solution: Step 1: Confirm HBV: well-established chronic carriage with HBsAg persistence.Step 2: Confirm HCV: high chronicity rates in untreated infections.Step 3: Confirm HDV: dependent on HBV; chronic coinfection/superinfection documented.Step 4: Conclude “All of these.” Verification / Alternative check: Clinical guidance emphasizes screening for chronic HBV/HCV, and managing HDV in HBV carriers due to higher severity and progression rates. Why Other Options Are Wrong: Single-virus choices understate the breadth of chronicity among bloodborne hepatitis viruses. HAV only: HAV does not become chronic; it is acute and self-limited. Common Pitfalls: Assuming dependency (HDV on HBV) precludes chronicity; confusing HAV/HEV (generally non-chronic) with bloodborne agents. Final Answer: All of these.

Question 15

HBV–HDV interactions – Identify the most serious clinical scenario among the following combinations of infection.

Accepted Answer

Introduction: Outcomes of hepatitis D virus (HDV) infection depend on whether it occurs alongside primary HBV infection (coinfection) or in an existing HBV carrier (superinfection). Understanding which scenario is most severe guides prevention and counseling of HBsAg carriers. Given Data / Assumptions: HDV requires HBsAg from HBV to assemble infectious particles. Coinfection = simultaneous acute HBV and HDV acquisition. Superinfection = HDV acquisition in a chronic HBV (HBsAg) carrier. Concept / Approach: Compare clinical severity and chronicity risk. Coinfection often presents as acute hepatitis with higher chance of resolution. Superinfection occurs on a background of established HBV, often leading to severe hepatitis, rapid progression, and higher risk of chronic HDV infection with decompensation. Step-by-Step Solution: Step 1: Define coinfection vs superinfection.Step 2: Review outcomes: coinfection → higher clearance; superinfection → severe disease and chronicity.Step 3: Identify superinfection as the most serious scenario.Step 4: Select option naming superinfection of an HBsAg carrier by HDV. Verification / Alternative check: Clinical series and exam keys consistently rank HDV superinfection as more severe, with increased risk of fulminant hepatitis and chronic advanced liver disease. Why Other Options Are Wrong: HBV alone: generally less severe than HDV superinfection. Coinfection: acute but higher chance of recovery without chronicity. None: incorrect; a clear most-serious option exists. HEV in HBV carriers: can be severe but the question compares HDV-specific interactions. Common Pitfalls: Confusing coinfection with superinfection; underestimating the impact of preexisting HBsAg on HDV replication. Final Answer: Superinfection of an HBsAg carrier by HDV.

Question 16

HBV antigens – Identify which antigen is located in the viral envelope of hepatitis B virus.

Accepted Answer

Introduction: Hepatitis B virus (HBV) particles contain distinct antigens that are used in diagnosis and indicate different stages of infection. Knowing which antigen resides in the envelope is critical for interpreting serology and understanding HDV dependency on HBV for envelope proteins. Given Data / Assumptions: HBV structure includes an envelope, a nucleocapsid, and genomic DNA. Surface antigen (HBsAg) forms the envelope spikes and subviral particles. Core and e antigens are internal/secreted markers, not envelope spikes. Concept / Approach: Map antigens to virion components: the envelope is composed of lipids and HBsAg proteins (L, M, S). The core (HBcAg) encloses the genome and polymerase. HBeAg is a secreted derivative of the core/precore region, serving as a marker of replication, not a structural envelope component. Step-by-Step Solution: Step 1: Identify envelope proteins as HBsAg.Step 2: Exclude core-associated antigens (HBcAg, HBeAg) from the envelope.Step 3: Note HBx as a regulatory protein, not a major virion structural antigen.Step 4: Select HBsAg for the envelope. Verification / Alternative check: Laboratory detection of HBsAg indicates presence of HBV surface proteins in blood, matching its role as an envelope component and explaining formation of abundant noninfectious HBsAg spheres/filaments. Why Other Options Are Wrong: HBcAg/HBeAg: nucleocapsid or secreted markers; not envelope proteins. HBxAg: regulatory; not a defining envelope antigen. Precore only: pertains to HBeAg synthesis; not envelope. Common Pitfalls: Equating abundant serum HBeAg with structural envelope location; misplacing HBx in the virion structure. Final Answer: HBsAg (surface antigen).

Question 17

Hepatitis A – Identify the statement that is NOT correct regarding HAV characteristics and disease outcomes.

Accepted Answer

Introduction: Hepatitis A virus (HAV) is an enterically transmitted picornavirus that causes acute, self-limited hepatitis. Understanding what HAV does not do helps distinguish it from HBV and HCV, which are associated with chronicity and hepatocellular carcinoma (HCC). This question asks you to identify the incorrect statement about HAV. Given Data / Assumptions: HAV is non-enveloped, environmentally hardy, and transmitted fecal–orally. Cell-culture propagation is possible in specific primate/human lines. HAV does not lead to chronic hepatitis or HCC. Concept / Approach: Contrast HAV with oncogenic hepatitis viruses. HAV causes acute disease with full recovery and lifelong immunity in most cases. It lacks integration mechanisms and chronic inflammatory milieu typical of HBV/HCV-associated carcinogenesis. Identify the statement claiming HCC causation as the incorrect one. Step-by-Step Solution: Step 1: Confirm HAV's environmental stability: resistant to mild heat, acid, and detergents.Step 2: Confirm fecal–oral transmission via contaminated food/water.Step 3: Recognize that cell culture growth, while specialized, is documented.Step 4: Flag the claim linking HAV to HCC as incorrect; HAV is not oncogenic. Verification / Alternative check: Oncovirology references attribute HCC risk to chronic HBV/HCV (and synergistic factors), not HAV. Public health messaging focuses on sanitation and vaccination rather than cancer prevention for HAV. Why Other Options Are Wrong: Growth in culture: achievable in appropriate systems. Environmental stability: consistent with non-enveloped structure. Fecal–oral transmission: hallmark of HAV spread. None of the above: incorrect because one statement (HCC causation) is indeed wrong. Common Pitfalls: Projecting oncogenicity of HBV/HCV onto HAV; assuming all hepatitis viruses share similar chronic outcomes. Final Answer: HAV infection may cause hepatocellular carcinoma (HCC).

Question 18

Specimens harboring HBV – Identify which body fluids/tissues may contain hepatitis B virus in an infected person.

Accepted Answer

Introduction: Understanding which specimens can harbor hepatitis B virus (HBV) informs transmission risk, infection control, and counseling. HBV is a bloodborne virus, but infectious virions and HBsAg can also be present in other body fluids. Given Data / Assumptions: HBV circulates at high titers in blood of infected persons, especially in HBeAg-positive states. Sexual transmission implicates semen and vaginal secretions. HBV DNA and HBsAg can be detected in saliva; although transmission risk is lower than blood exposure, presence is documented. Concept / Approach: List fluids with demonstrated HBV presence and potential infectivity. When multiple relevant specimens are enumerated (blood, semen, saliva), the comprehensive choice is “All of these.” Step-by-Step Solution: Step 1: Confirm blood as the principal reservoir for transmission (transfusion, needlesticks).Step 2: Confirm semen as a vehicle for sexual transmission.Step 3: Confirm detection of HBV markers in saliva, supporting potential albeit lower risk.Step 4: Choose the inclusive option. Verification / Alternative check: Infection control guidelines list blood and certain body fluids, including semen and, to a lesser extent, saliva, as relevant for HBV presence. Vaccination and standard precautions remain key. Why Other Options Are Wrong: Single-fluid choices understate HBV distribution. None of these: contradicted by robust virologic evidence. Common Pitfalls: Assuming saliva cannot harbor HBV; ignoring that infectivity varies by fluid and viral load. Final Answer: All of these.

Question 19

The development of hepatocellular carcinoma (HCC) is associated with which hepatitis/hepadnavirus agents? (Consider established human and animal models that demonstrate oncogenic association.)

Accepted Answer

Introduction: Hepatocellular carcinoma (HCC) is a primary liver cancer strongly linked to chronic hepatitis B virus (HBV) infection in humans. Closely related hepadnaviruses in animal models—including woodchuck hepatitis virus (WHV) and ground squirrel hepatitis virus (GSHV)—provide experimental evidence for the oncogenic potential of this virus family. Given Data / Assumptions: HBV is a hepadnavirus with partially double-stranded DNA. Chronic infection and integration events are implicated in oncogenesis. Animal hepadnaviruses (WHV, GSHV) cause HCC in their respective hosts. Concept / Approach: Persistent hepadnavirus infection promotes carcinogenesis through chronic inflammation, regenerative hyperplasia, and viral DNA integration near host oncogenes or tumor suppressor loci. HBx protein–mediated transcriptional dysregulation also contributes to malignant transformation. Step-by-Step Solution: Identify human association: HBV infection elevates lifetime HCC risk. Corroborate with animal models: WHV in woodchucks and GSHV in ground squirrels reproducibly lead to HCC. Synthesize: All listed agents (human and animal hepadnaviruses) are associated with HCC development in their hosts. Select the comprehensive option that captures all true associations. Verification / Alternative check: Longitudinal cohort data in endemic regions link chronic HBV to HCC; laboratory colonies of woodchucks chronically infected with WHV develop HCC at high frequency, reinforcing causality. Why Other Options Are Wrong: Ground squirrel / Woodchuck virus alone: Each is associated, but not the complete answer. HBV alone: True but incomplete given the question's scope. Common Pitfalls: Assuming only human evidence matters; animal hepadnavirus models are foundational to understanding HBV oncogenesis. Final Answer: all of the above are associated with hepatocellular carcinoma in their respective hosts.

Question 20

Which of the following hepatitis viruses is NOT an RNA virus? (Identify the DNA virus among common hepatitis agents.)

Accepted Answer

Introduction: Most hepatitis viruses are RNA viruses, but one major exception exists. This question tests recognition of the unique nucleic acid type that distinguishes hepatitis B virus (HBV) from other hepatitis agents. Given Data / Assumptions: HAV, HEV, and HGV (GB virus C) are RNA viruses. HBV belongs to the Hepadnaviridae family and possesses DNA. Classification is based on genome type, not clinical syndrome severity. Concept / Approach: HBV contains a partially double-stranded, circular DNA genome and replicates via reverse transcription. In contrast, HAV (Picornaviridae), HEV (Hepeviridae), and HGV/GBV-C (Flaviviridae-related) carry single-stranded RNA genomes. Step-by-Step Solution: List genome types for each candidate. Single out the DNA-containing virus (HBV). Confirm others are RNA viruses. Choose the only non-RNA option. Verification / Alternative check: Standard virology references classify HBV as a DNA virus with reverse transcriptase activity. Why Other Options Are Wrong: Hepatitis A / E / G: All are RNA viruses. Common Pitfalls: Confusing replication via reverse transcriptase (seen in HBV) with RNA genome possession; HBV is still a DNA virus. Final Answer: Hepatitis B virus is not an RNA virus.

Hepatitis Viruses Questions