A pathophysiology and psychosocial diagram illustrating the impact of chronic Hepatitis B virus (HBV) infection on an individual. The central element is a black silhouette of a person, representing an individual living with chronic hepatitis B (CHB). To the top-left, a diagram of the HBV virus particles indicates the clinical origin of the condition. Red jagged arrows point from the virus and a group of blue-toned human figures toward the central individual, symbolizing external stressors. The diagram categorizes the consequences into three tiers: 'Primary impacts' (fear of progression, financial loss, fear of transmission); 'Secondary impacts' originating from the community and healthcare providers (stigma and discrimination); and 'Tertiary impacts' shown on the right (silence, loneliness, withdrawal from society, self-stigma, and passivity). The visual logic demonstrates how biological disease leads to societal reaction, which ultimately results in negative psychological internalizations for the patient. This educational infographic is designed for clinicians and public health educators to understand the multifaceted lived experience of CHB beyond clinical markers.

This pathophysiology flow diagram illustrates the development of Woodchuck Hepatitis Virus (WHV) infections, serving as a preclinical model for human Hepatitis B virus (HBV). The diagram categorizes outcomes based on viral load (WHV dose), sites of infection, serological profiles, and pathological outcomes. A low dose (≤ 10^3 virions) primarily targets the immune system, leading to Primary Occult Infection (POI) characterized by a sero-negative profile (WHsAg-, Anti-WHc-, Anti-WHs-) despite WHV DNA persistence. This may progress to hepatocellular carcinoma (HCC) in ~20% of cases. A secondary pathway for low doses involves the lymphatic system and liver, leading to Secondary Occult Infection (SOI) with a sero-positive profile (WHsAg-, Anti-WHc+, Anti-WHs +/-). Higher doses (≥ 10^3 virions) concurrently infect the immune system and liver, presenting as sero-positive (WHsAg+, Anti-WHc+, Anti-WHs-). These infections lead to either Resolved Acute Hepatitis (SLAH), which transitions to SOI, or Chronic Hepatitis (CH). CH carries a high risk of HCC (~90%). The chart emphasizes the persistence of viral DNA across all outcomes despite differing serological markers.

Summary : This figure presents two line plots showing the typical serologic courses of acute and chronic hepatitis B virus (HBV) infection, comparing the progression and recovery of serologic markers over time. line plot: # Panel A: Typical serologic course of acute HBV infection to recovery ## Title & Axes : • Title: "A. Typical serologic course of acute HBV infection to recovery" • X-axis: "Weeks after exposure" (tick labels: 0, 4, 8, 12, 16, 20, 24, 28, 32, 36, 52, 100) • Y-axis: "Relative concentration" (no explicit tick labels) • Additional timeline annotations: "HBV DNA", "Symptoms", "HBeAG", "Anti-HBe" (horizontal arrows above plot) ## Data Points : • HBsAg (solid line): Rises sharply after exposure, peaks around 8–12 weeks, then declines and disappears by ~24–28 weeks. • Total anti-HBc (dashed line): Rises after exposure, peaks around 16–20 weeks, remains elevated beyond 100 weeks. • IgM anti-HBc (dotted line): Rises after exposure, peaks around 12–16 weeks, declines and disappears by ~28–32 weeks. • Anti-HBs (long dashed line): Appears after ~24–28 weeks, rises and remains elevated beyond 100 weeks. ## Design Encodings : • HBsAg: solid purple line • Total anti-HBc: dashed purple line • IgM anti-HBc: dotted purple line • Anti-HBs: long dashed purple line • All lines plotted against the same axes; no log scale or error bars. ## Distribution & Trends : • HBsAg and IgM anti-HBc both show transient peaks and then decline. • Total anti-HBc and anti-HBs persist long-term after recovery. # Panel B: Typical serologic course of progression to chronic HBV infection ## Title & Axes : • Title: "B. Typical serologic course of progression to chronic HBV infection" • X-axis: "Weeks after exposure" (tick labels: 0, 4, 8, 12, 16, 20, 24, 28, 32, 36, 52), then "Years" (break in axis) • Y-axis: "Relative concentration" (no explicit tick labels) • Additional timeline annotations: "HBV DNA", "Acute (6 months)", "Chronic (years)", "HBeAG", "Anti-HBe" (horizontal arrows above plot) ## Data Points : • HBsAg (solid line): Rises after exposure, remains persistently elevated for years. • Total anti-HBc (dashed line): Rises after exposure, remains persistently elevated for years. • IgM anti-HBc (dotted line): Rises after exposure, peaks around 12–16 weeks, declines and disappears by ~28–32 weeks. ## Design Encodings : • HBsAg: solid purple line • Total anti-HBc: dashed purple line • IgM anti-HBc: dotted purple line • All lines plotted against the same axes; no log scale or error bars. ## Distribution & Trends : • HBsAg and total anti-HBc remain persistently elevated in chronic infection. • IgM anti-HBc is transient and disappears after the acute phase. # Analysis : • In acute HBV infection (Panel A), HBsAg and IgM anti-HBc are transient, while total anti-HBc and anti-HBs persist after recovery, indicating resolution and immunity. • In chronic HBV infection (Panel B), HBsAg and total anti-HBc remain persistently elevated for years, while IgM anti-HBc is only present during the acute phase, indicating ongoing infection without resolution. • The presence and duration of serologic markers distinguish acute recovery from progression to chronic infection.