Hepatitis B and C in sexual health

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

A hepatitis result in sexual health creates three immediate questions: is infection current, is the patient or a contact still preventably susceptible, and who owns the next step? HBV and HCV share liver consequences but require different marker logic and different prevention after exposure.

For HBV, HBsAg, total anti-HBc and anti-HBs are interpreted together. HBsAg points to current infection, anti-HBc proves natural exposure and anti-HBs records immunity. This separates vaccine-only immunity from resolved infection and susceptibility. HBV DNA, ALT and fibrosis assessment then inform specialist phase classification; no single marker decides chronic treatment.

For HCV, antibody answers whether exposure has occurred but may remain reactive after spontaneous clearance or successful treatment. Reflex RNA prevents a reactive screening result from becoming a diagnostic dead end: detectable RNA means current viraemia, while undetectable RNA usually means no current infection unless the exposure is too recent for that conclusion.

Transmission counselling must preserve the difference between the viruses. HBV is readily transmitted sexually and through blood. HCV transmission is dominated by blood exposure; sexual risk rises with practices and settings that involve mucosal trauma or blood, including some chemsex and injecting contexts, HIV coinfection and ulcerative STI.

Prevention after exposure also diverges. HBV vaccine provides active protection and HBIG adds temporary passive protection for defined high-risk situations. HCV has neither vaccine nor immunoglobulin and routine antiviral PEP is not used, so the response is baseline testing, scheduled early RNA detection, harm reduction and rapid treatment if viraemia appears.

The clinic should not stop at notification of a reactive result. Current HBV needs hepatology assessment, contact testing and vaccination, pregnancy planning and reactivation precautions. Current HCV should move promptly to direct-acting antiviral assessment. Drug, dose and duration remain decisions for the dedicated treatment guideline and specialist team.

Key points

HBV spreads efficiently through sexual and blood exposure; HCV is chiefly blood-borne, with sexual transmission concentrated where blood, mucosal trauma, injecting, HIV or ulcerative STI is present.
Read HBV as a three-marker pattern: HBsAg indicates current infection, anti-HBc records natural exposure and anti-HBs indicates immunity; vaccination produces anti-HBs without anti-HBc.
A reactive anti-HCV result records exposure, not current infection; reflex HCV RNA or a validated core-antigen route establishes active viraemia.
After a recent exposure, one negative antibody result may be too early: follow the virus- and assay-specific schedule and use HCV RNA when early detection is required.
For a susceptible person after significant HBV exposure, give vaccine promptly and use the Green Book and UKHSA criteria to decide whether HBIG is also required.
HCV has no vaccine or immunoglobulin, and routine direct-acting antiviral post-exposure prophylaxis is not recommended.
Refer HBsAg-positive people for HBV phase, fibrosis and treatment assessment, and link detectable HCV RNA directly to curative specialist care.
Include HIV, site-specific STI testing, pregnancy, partner care and harm reduction according to exposure, while avoiding assumptions based on identity.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

HBV sexual and blood transmission

HBV is present in infectious blood and genital secretions and can cross mucosa or broken skin during sex, injecting, needlestick or shared personal equipment exposure.

HCV blood inoculation

HCV transmission chiefly requires infected blood to enter another person’s circulation, making shared injecting equipment and other blood exposures central to the history.

Context-dependent sexual HCV risk

Sexual transmission becomes more relevant where practices cause mucosal trauma or blood exposure and in networks affected by injecting, HIV or ulcerative STI.

Perinatal exposure

Both viruses may be transmitted around birth, but HBV has a time-critical neonatal vaccine and, for defined maternal risk, HBIG prevention pathway.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Persistent HBV template
HBV establishes stable nuclear viral DNA in hepatocytes and replicates through reverse transcription, so available treatment can suppress replication without reliably eliminating reactivation potential.
2
Current HCV is defined by viraemia
HCV is an RNA virus; circulating RNA demonstrates active infection, whereas antibody records immune recognition and may remain after virus has cleared.
3
Host response injures the liver
Much of the hepatocyte damage in viral hepatitis reflects immune activity against infected cells, allowing infection to be clinically silent, inflammatory or occasionally fulminant.
4
Chronic injury remodels the liver
Ongoing necroinflammation promotes fibrosis and cirrhosis, which drives portal hypertension, loss of synthetic reserve and continuing hepatocellular-carcinoma risk.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Acute HBV illness

Fever, anorexia, nausea, arthralgia, right-upper-quadrant discomfort, dark urine and jaundice can follow recent HBV exposure, sometimes after a rash and polyarthralgia prodrome.

HBV found by screening

An HBsAg-positive person may feel entirely well, so the result still requires complete markers, HBV DNA, liver assessment and referral rather than reassurance from a normal examination.

HCV exposure without symptoms

Most people identified after injecting, occupational or sexual blood exposure have no specific clinical syndrome; testing history is therefore more sensitive than symptom screening.

Possible acute HCV

Fatigue, nausea, abdominal discomfort, dark urine or jaundice may occur after exposure but are uncommon and cannot distinguish HCV from other hepatitic illnesses.

Established chronic liver diseaseRed flag

Thrombocytopenia, splenomegaly, spider naevi, ascites or abnormal synthetic function may reveal advanced HBV or HCV even after years of few symptoms.

Acute liver failureRed flag

Encephalopathy, coagulopathy, hypoglycaemia, bleeding or rapid multiorgan deterioration requires emergency liver and transplant-centre involvement.

Red flags requiring action

Jaundice with confusion, asterixis, bleeding, hypoglycaemia or deteriorating coagulation requires emergency liver-failure care.
HBsAg positivity in pregnancy needs prompt HBV DNA assessment and a documented plan for maternal care and neonatal immunoprophylaxis.
An infant born to an HBsAg-positive mother must receive hepatitis B vaccine within 24 hours and HBIG when the current national criteria apply.
Chemotherapy, major immunosuppression or B-cell-depleting treatment must not begin before HBsAg and anti-HBc results have been reviewed and reactivation prevention assigned.
A sudden ALT rise or jaundice in chronic HBV requires assessment for disease activity, reactivation, adherence, drug injury and hepatitis D.
A recent sexual, injecting, occupational or household blood exposure needs same-day assessment because hepatitis B vaccine and selected HBIG are time sensitive.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
HBsAg, total anti-HBc and anti-HBs panelFirst step
Why
Assign the patient to current HBV infection, resolved natural infection, vaccine immunity or susceptibility.
Interpretation and limitations
HBsAg indicates current infection; anti-HBc means natural exposure; anti-HBs means immunity. Read the combination, and repeat or add HBV DNA when a recent exposure or isolated result remains unresolved.
02
HBV DNA, HBeAg and liver profile
Why
Describe viral replication and provide the information needed for specialist phase and transmission assessment.
Interpretation and limitations
HBV DNA is interpreted with ALT, fibrosis and clinical context. HBeAg or a single normal ALT cannot independently rule treatment in or out.
03
Anti-HCV with reflex HCV RNA
Why
Use one screening pathway to identify both previous exposure and whether viraemia is present now.
Interpretation and limitations
Reactive antibody plus detectable RNA is current HCV. Reactive antibody with undetectable RNA means no current viraemia unless the exposure is sufficiently recent to require repeat RNA.
04
Early HCV RNA after recent exposure
Why
Look for infection during the period before antibody may become reactive.
Interpretation and limitations
A very early negative RNA result does not end follow-up; use the schedule for the particular occupational, injecting or sexual-health exposure.
05
Severity and fibrosis assessment
Why
Separate a stable outpatient result from synthetic failure, portal hypertension or treatment urgency.
Interpretation and limitations
Use bilirubin, albumin, INR, platelet count and non-invasive fibrosis assessment as appropriate; ALT alone does not stage liver damage or exclude important disease.
06
Coinfection, pregnancy and exposure-site tests
Why
Identify factors that change prevention, urgency or treatment selection.
Interpretation and limitations
Test HIV and relevant STIs, assess HAV and HBV immunity as appropriate, and coordinate any HBsAg-positive pregnancy with maternity, hepatology and neonatal services.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Resolved HBV infection

Absent HBsAg with both anti-HBc and anti-HBs usually records past natural infection and immunity, although reactivation risk remains relevant before immunosuppression.

Vaccine-derived HBV immunity

Anti-HBs without anti-HBc supports vaccine-derived immunity because hepatitis B vaccination presents surface antigen without exposing the person to viral core antigen.

Cleared or cured HCV

Reactive antibody with undetectable RNA indicates no current viraemia in the absence of a very recent exposure requiring repeat testing.

Another cause of hepatitis

HAV, HEV, HDV, drug injury, alcohol-related injury and other viral or metabolic causes can produce the same jaundice and enzyme pattern, so virus-specific tests are essential.

Occult or window-period infection

Recent exposure may precede marker positivity, and low-level HBV DNA can occasionally persist without HBsAg; timing and immune context determine additional testing.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01RESULTSTurn screening markers into two diagnosesFirst stepThe laboratory reports HBsAg positivity and reactive anti-HCV in the same asymptomatic patient.

1Complete the HBV marker panel, arrange HBV DNA and liver or fibrosis assessment, and refer current HBV through the named pathway.
2Reflex the anti-HCV sample to RNA because antibody cannot distinguish current infection from previous clearance or cure.
3Assess jaundice, synthetic failure, pregnancy, HIV, other STIs, medicines, alcohol and ongoing exposure without delaying either referral.
4Explain the viruses separately, identify susceptible contacts who need HBV vaccination and give the patient a named follow-up owner for every pending result.

02HBV EXPOSUREUse prevention while it can still workA susceptible person reports a recent sexual or blood exposure to someone with current hepatitis B.

1Record the exposure type and date, the source HBsAg status and the exposed person’s vaccine course and documented antibody response.
2Give hepatitis B vaccine as soon as possible, ideally within 48 hours and still consider it up to seven days after a single exposure.
3Check the Green Book and current UKHSA immunoglobulin criteria for that exact exposure to decide whether HBIG is also indicated.
4Complete vaccination, schedule follow-up infection testing and give interim sexual or blood-safety advice appropriate to the exposure.

03HCV EXPOSUREPlan detection because there is no PEPA needlestick, shared equipment or sexual exposure involving blood could have transmitted hepatitis C.

1Provide immediate wound care where relevant, document the event, obtain baseline HCV, HBV and HIV tests and assess the source lawfully.
2Explain that HCV has no vaccine or immunoglobulin and that direct-acting antivirals are not routinely prescribed as post-exposure prophylaxis.
3Schedule early HCV RNA and later follow-up using the current route-specific timetable, rather than relying on symptoms or one early antibody test.
4If RNA becomes detectable, link directly to treatment and reinforce safer injecting, equipment and sexual practices without requiring abstinence for access.

04LINKAGEKeep ownership until specialist care startsHBsAg or HCV RNA confirms a current viral infection.

1EscalationAssess bilirubin, INR, albumin, platelets, fibrosis and features of decompensation, and escalate jaundice with bleeding, confusion or ascites urgently.
2Refer HBV for hepatology phase-specific treatment and monitoring and HCV for specialist direct-acting antiviral selection; the sexual-health result does not determine a universal medicine, dose or duration.
3Provide HIV and coinfection testing, pregnancy assessment and a complete interaction and medicine history for the receiving service.
4Close the prevention loop with partner testing, HBV vaccination, harm reduction and ongoing liver or cancer surveillance appropriate to the virus and fibrosis stage.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Provides long-term suppression when HBV phase, liver injury, fibrosis and the wider clinical context meet treatment criteria.

Specialist-selected chronic hepatitis B antiviral

HBsAg-positive adults need hepatology assessment and dose selection under the dedicated HBV treatment guideline; sexual-health assessment alone does not determine a universal regimen.

Choice and duration depend on compensated or decompensated disease, renal and bone function, pregnancy, previous antiviral exposure or resistance and HIV coinfection. HIV coinfection needs a fully suppressive ART combination with adequate HBV activity.

Uses a context-matched direct-acting antiviral combination to cure current HCV viraemia.

Specialist-selected hepatitis C direct-acting antiviral regimen

Detectable HCV RNA requires specialist selection of the combination and duration under the dedicated HCV treatment guideline.

Regimen and duration depend on liver compensation, previous treatment or failure, renal function, pregnancy, HBV or HIV coinfection and medicine interactions; use the current dedicated HCV treatment body.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute liver failure

Severe acute or reactivated hepatitis can cause coagulopathy, encephalopathy, hypoglycaemia, renal injury and multiorgan deterioration requiring transplant-centre discussion.

Cirrhosis and portal hypertension

Chronic HBV or HCV may progress to fibrosis, ascites, variceal bleeding, encephalopathy and reduced hepatic reserve.

Hepatocellular carcinoma

Long-term viral and inflammatory injury increases primary liver-cancer risk, so surveillance may continue after suppression or cure when the fibrosis or HBV risk profile qualifies.

HBV reactivation

Loss of immune control during chemotherapy or immunosuppression can restore clinically important HBV replication even after apparently resolved infection.

Onward transmission or reinfection

Unrecognised HBV or HCV viraemia exposes partners and contacts; after HCV cure, another blood exposure can cause a new infection because protective immunity is not established.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Track every reactive screen through to a complete HBV pattern or an HCV RNA result; antibody notification alone is unfinished care.
After recent exposure, document the assay-specific testing timetable and who will recall the patient for each sample.
For hepatitis B prevention, record vaccine dates, product or schedule and post-vaccination serology when the Green Book calls for it.
For current infection, monitor liver injury, synthetic function, platelets and fibrosis within the responsible hepatology pathway.
After HCV therapy, document sustained virological response with HCV RNA at least 12 weeks after treatment.
Continue hepatocellular-carcinoma surveillance when cirrhosis or another qualifying risk remains despite HBV suppression or HCV cure.
Where blood exposure continues, offer repeat HCV RNA because persistent antibody neither detects reinfection nor provides immunity.
Before immunosuppression or chemotherapy, make HBV marker review and the reactivation prevention plan visible to the prescribing team.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

HBV markers answer different questions

Surface antigen asks whether infection is current, core antibody whether natural exposure occurred, and surface antibody whether immunity is present.

Vaccination has a recognisable signature

Anti-HBs without anti-HBc fits vaccine-derived immunity because the vaccine does not contain core antigen.

HCV antibody can outlive infection

Reactive anti-HCV may persist after clearance or cure, so RNA rather than repeat antibody determines whether virus circulates now.

Normal enzymes do not close the case

A normal ALT does not exclude current infection or significant fibrosis and cannot replace viral markers and staging.

Only HBV has post-exposure immunoprophylaxis

Vaccine and selected HBIG can prevent HBV, whereas HCV exposure is managed through scheduled RNA detection and rapid treatment of infection.

HCV cure is not a vaccine

Successful treatment clears viraemia but does not protect against another infection, so ongoing exposure still requires harm reduction and repeat RNA testing.

A reactive result needs an owner

Named linkage reduces the risk that an asymptomatic patient receives a result but never completes staging, vaccination of contacts or curative care.

11Common pitfallsFrequent interpretation and management errors.

01
Calling HBV status from HBsAg, anti-HBc or anti-HBs in isolation when the complete pattern is available.
02
Labelling reactive anti-HCV as active infection without an RNA or validated core-antigen result.
03
Using one negative early antibody test to end follow-up after a recent exposure.
04
Delaying hepatitis B vaccine while waiting for symptoms or a later clinic appointment.
05
Transferring HBIG or vaccine logic from HBV to HCV, or prescribing routine HCV antiviral PEP.
06
Treating HBV and HCV sexual-transmission risk as identical rather than asking about blood, trauma, injecting and ulcerative STI.
07
Selecting chronic antiviral drugs from the screening visit without the dedicated treatment guideline, fibrosis stage, pregnancy, coinfection and interaction review.
08
Discharging a reactive result without named linkage, contact prevention and a plan for every outstanding test.

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