Hepatitis C Testing Before Treatment: Genotype, Viral Load and Liver Fibrosis Scans

The letter said the antibody result was positive, and then it said almost nothing else. Maria read it twice at the kitchen table, once quickly and once slowly, looking for the word she wanted, which was done. Instead it listed more appointments: a second blood draw, something called a hepatitis C genotype test, a scan of her liver she had never heard of. She felt well. She had felt well for years. Why, she wondered, did a virus she couldn’t feel need this much paperwork?

It is a fair question, and the answer is reassuring in its own way. Modern hepatitis C treatment is short and tablet-based, and the tests that come before it exist so that the course can be chosen carefully rather than guessed. Each result answers a different question: Is the virus still there? How much of it? Which strain? And what has it already done to the liver?

This explainer walks through those questions in the order a clinic usually asks them, so the next letter reads less like a puzzle and more like a plan.

What does a hepatitis C genotype test actually tell you?

Hepatitis C is not a single virus so much as a family of close relatives. Scientists sort those relatives into genotypes, which are groups of strains that share a similar genetic code, numbered 1 through 6 with rarer types described since. Within each genotype sit subtypes, written as a letter after the number, such as 1a or 1b. A hepatitis C genotype test reads a stretch of the virus’s genetic material from a blood sample and reports which group and subgroup it belongs to.

Two things about that result surprise people. First, the genotype is fixed. You acquire a particular strain at the time of infection, and it stays the same for as long as the virus is present; it does not drift from type 2 to type 3 over the years. Second, the genotype says nothing about how unwell you are or how damaged your liver is. Someone with genotype 1a may have a healthy liver, while someone with the same subtype may have cirrhosis. Damage depends on time, alcohol, other liver conditions and individual biology, not on the virus’s family tree.

Where genotype does matter is treatment planning. Different strains respond somewhat differently to different antiviral combinations, and knowing the type helps the prescribing team match the regimen and its length to the person in front of them. Geography shapes what turns up: in the United States, genotype 1 accounts for roughly three quarters of infections according to the CDC, while other regions see more genotype 3 or 4. Your result is one input among several, and the treating team weighs it alongside viral load, fibrosis stage and your other medicines before recommending anything.

Why test before treating hepatitis C at all?

If the medicines work well across most strains, a reasonable person might ask why the clinic doesn’t simply prescribe them the day the antibody result comes back. The short answer is that treatment is chosen for a specific liver, not for a lab value, and several things must be known first.

The first is whether the infection is still active. A positive antibody test means the immune system has encountered the virus at some point; it cannot distinguish a current infection from one the body cleared on its own years ago. The World Health Organization estimates that about 30% of people infected clear the virus spontaneously within six months, leaving antibodies behind but no virus to treat. Prescribing for them would expose them to medicine they do not need.

The second is what shape the liver is in. WHO notes that among people who develop chronic infection, an estimated 15% to 30% progress to cirrhosis within 20 years, and cirrhosis changes the picture: it can alter which regimen is suitable, how long it runs, and what monitoring must continue afterwards, including surveillance for liver cancer even once the virus is gone.

The third is safety. Direct-acting antivirals, the tablet-based medicines that block specific viral proteins, interact with a range of common prescriptions and can trigger flare-ups of hepatitis B in people who carry that second virus quietly. Kidney function, pregnancy status and current medications all need checking. None of this is bureaucratic caution for its own sake. Each test closes off a way the treatment could go wrong, so that a course lasting a few weeks gives the best chance of clearing the virus for good.

Hepatitis C antibody vs RNA test: which one confirms infection?

The first test almost everyone receives looks not for the virus but for the body’s reaction to it. The antibody test detects proteins the immune system makes in response to hepatitis C. It is inexpensive to run, widely available and a sensible first screen, which is why the CDC recommends it once for every adult and during every pregnancy. Its limitation is memory: antibodies persist for life, so a positive result flags past exposure without confirming the virus is still there.

That confirmation comes from the RNA test, sometimes called a PCR or nucleic acid test. It searches directly for the virus’s genetic material. A detectable result means active infection; an undetectable result after a positive antibody test usually means the body cleared the virus on its own, or that a previous treatment worked. The CDC describes this two-step sequence, antibody followed by RNA, as the standard diagnostic pathway, and many laboratories now run the RNA test automatically on the same sample when the antibody comes back positive, sparing a second appointment.

Timing explains the occasional confusing result. After a fresh exposure, RNA becomes detectable within a week or two, while antibodies take longer to appear; the CDC gives a typical window of eight to eleven weeks for antibodies to develop. Someone tested very early after exposure could therefore have a negative antibody test and a positive RNA test at the same time. Clinicians who suspect recent exposure sometimes order RNA directly for this reason.

People also ask whether a repeat antibody test years after successful treatment means the virus is back. It does not. The antibody remains as a permanent record; only the RNA test can answer whether the virus is present now.

Hepatitis C viral load meaning: what the number tells you and what it doesn't

When the RNA test is positive, the laboratory reports a quantity: the viral load, which is the amount of viral genetic material in a set volume of blood, expressed as international units per milliliter. The figures can be startling, often running into the hundreds of thousands or millions. Patients frequently read a high number as a sign of severe disease and a low one as a sign they have got off lightly. Neither reading holds up.

Viral load in hepatitis C does not track with liver damage. Someone with a modest number can have advanced scarring; someone with a very high number can have a liver that looks almost normal on scanning. The virus’s effect comes from decades of low-grade inflammation, not from the sheer count on any given day, and the count itself fluctuates. Mayo Clinic notes that the quantity is measured mainly to establish a baseline, not to grade illness.

That baseline is the number’s real purpose. Before treatment it documents that the virus is present and gives a starting point. During and after treatment, repeat measurements show whether the medicines are doing their job. The result the treating team is ultimately looking for is sustained virological response, defined as undetectable virus in the blood measured 12 weeks after the last dose. Reaching that point indicates the infection has been cleared, and the NHS describes this 12-week check as the standard confirmation.

A practical implication follows. If your viral load is high, you are not sicker than your neighbor with a lower one, and you are not less likely to respond to treatment. Ask instead about your fibrosis stage, which is the number that actually reflects the liver’s condition.

How the hepatitis C genotype test works, step by step

The process begins the same way as every other blood test: a needle in the arm, a tube or two filled, a bandage. Nothing about the draw itself feels different, and no fasting or preparation is needed. What differs is what happens to the sample afterwards.

In the laboratory, technicians first extract the virus’s RNA, its genetic material, from the blood. Because the amount is tiny, the genotype test relies on the same amplification method used for the viral load test: a chain reaction that copies a chosen segment of the viral genome many millions of times until there is enough to analyze. The segments chosen are regions where genotypes differ reliably from one another, typically parts of the genome that code for the virus’s structural or replication proteins.

From there, two approaches are common. One uses molecular probes designed to bind only to the pattern of a particular genotype, lighting up when they find a match. The other reads the actual sequence of genetic letters and compares it against a reference library. The report that comes back gives the genotype number and, where the method allows, the subtype letter.

The test needs detectable virus to work. If the viral load is very low, the laboratory may report an indeterminate or untypable result, and the treating team will decide whether to repeat it or proceed with a regimen that covers all genotypes. Mixed infections with two genotypes at once are described but uncommon. Occasionally a clinician also requests resistance testing, which looks for small mutations in the virus that reduce a specific medicine’s effect; this is generally reserved for particular genotypes or for people whose previous treatment did not clear the virus.

Do you still need a genotype test with pan-genotypic treatment?

A decade ago the genotype dictated almost everything: which medicines, for how long, and how likely they were to work. Interferon-based treatment struggled badly with some strains and did better with others. Then came direct-acting antivirals, and later combinations described as pan-genotypic, meaning they are designed to work against all major genotypes. Understandably, patients now ask whether the genotype test has become a relic.

The honest answer is: it depends on where you are treated and on your circumstances. WHO recommends pan-genotypic regimens precisely because they simplify care and, in settings where genotype testing is expensive or slow, allow treatment to start without it. In some public health programs the test has been dropped from the routine pathway for people without cirrhosis and without prior treatment, on the reasoning that the regimen would be the same regardless of the result.

Many specialist services still order it, for a few practical reasons. Not every available regimen is pan-genotypic, and where a genotype-specific option is appropriate, knowing the strain opens that choice. Some genotypes, particularly genotype 3 in people with cirrhosis, are associated with different treatment considerations. Genotype also determines whether resistance testing is worth doing before certain regimens, and it helps interpret what happened if a first course does not clear the virus. Knowing the subtype can matter when a later treatment plan is being drawn up.

None of this makes one approach right and the other wrong. Guidelines from WHO, the CDC and national bodies allow both, and the choice reflects the medicines available locally and your clinical picture. If your clinic orders the test, it is because the result will inform a decision. If it does not, ask what regimen is being considered and why the genotype does not change it.

Liver fibrosis scan for hepatitis C: what a stiffness measurement shows

Of all the pre-treatment tests, the fibrosis scan is the one most people have never encountered, and the one that says most about their health. Fibrosis is scar tissue laid down in the liver after years of inflammation; cirrhosis is its most advanced form, where scarring has reorganized the organ’s structure. Neither causes symptoms until late, which is why a scan, rather than how you feel, is used to measure it.

The most widely used method is transient elastography, an ultrasound-based technique that measures liver stiffness. A probe placed on the skin over the right ribs sends a gentle mechanical pulse into the liver and tracks how fast the resulting wave travels. Scar tissue is stiffer than healthy tissue, so the wave moves faster through a fibrotic liver. The machine converts that speed into a stiffness value in kilopascals, and the operator takes around ten readings to produce a reliable average. The whole appointment typically takes minutes, involves no radiation and feels like a series of light flicks against the side.

Results are mapped onto a staging scale that runs from F0, no scarring, to F4, cirrhosis. The cut-offs between stages vary slightly by cause of liver disease and by machine, so the number is interpreted by a clinician rather than read straight off a chart. Cleveland Clinic and Mayo Clinic both describe elastography as the usual way to assess damage before treatment, with biopsy now reserved for unclear cases.

A few situations can distort readings: eating within a few hours beforehand, active inflammation with very high liver enzymes, fluid in the abdomen or significant obesity. Clinics usually ask you to fast briefly and may repeat the scan if the result does not fit the rest of the picture.

Fibrosis blood scores and when a biopsy still comes up

Not every clinic has an elastography machine, and not every liver reads clearly on one. Fibrosis can also be estimated from ordinary blood results using simple formulas, and these scores are often run before or alongside a scan.

The two most common are the APRI, which compares a liver enzyme level with the platelet count, and the FIB-4, which adds age and a second enzyme. Both rest on the same observation: as scarring advances, platelets tend to fall and enzyme patterns shift. Neither score gives a precise stage, but each is good at ruling out advanced disease when low and flagging it when high. Results in the middle are indeterminate, and that is usually when a scan or a specialist opinion is sought. Some laboratories also offer proprietary panels that combine several blood markers; these are used in the same triage role.

For decades, the definitive test was the liver biopsy, in which a needle removes a sliver of tissue for examination under a microscope. It remains the most direct look at the liver, and it can detect other conditions, such as fatty liver disease or iron overload, that a stiffness reading cannot. Against that stands a small but real risk of bleeding and pain, a day of recovery, and the fact that a sample of one small area may not represent the whole organ.

Mayo Clinic notes that biopsy is now used far less often, typically when non-invasive results conflict with each other or with the clinical picture, or when a second liver condition is suspected. If a biopsy is suggested to you, the useful questions are what specific uncertainty it would resolve and whether that answer would change the treatment plan.

What other blood tests come before hepatitis C treatment?

Genotype, viral load and fibrosis stage answer the questions about the virus and the liver. A further set of tests answers questions about you, and they are ordered because direct-acting antivirals, while generally well tolerated, are not prescribed in isolation.

The most consequential is screening for hepatitis B. Some people carry that virus in a dormant state without knowing it, and clearing hepatitis C can, in a small number of cases, allow hepatitis B to reactivate. Prescribing information for direct-acting antivirals carries a formal warning about this, and the CDC’s clinical guidance recommends checking hepatitis B status before starting. Where the second virus is present, the treating team plans monitoring or treatment for it in parallel.

An HIV test is standard, both because the two infections share transmission routes and because HIV medicines can interact with hepatitis C regimens. A kidney function panel matters because some antivirals are handled differently when the kidneys are impaired. A standard liver panel and full blood count give baseline enzyme, bilirubin, albumin and platelet values, which also feed into the fibrosis scores described above. Where pregnancy is possible, a pregnancy test is usual, since safety data in pregnancy remain limited and most services defer treatment until afterwards.

The final check is not a blood test at all but a conversation. Direct-acting antivirals interact with a surprising range of everyday products, including some acid-reducing medicines, certain cholesterol drugs, anticonvulsants and the herbal supplement St John’s wort. Bring a complete list of everything you take, prescribed or not, including vitamins and over-the-counter remedies. The pharmacist or clinician will review it before a regimen is confirmed, and any change to an existing medicine is theirs to recommend, not something to attempt on your own.

Who is usually treated promptly, and who is asked to wait?

Current guidance from WHO and national bodies takes an expansive view: nearly everyone with chronic hepatitis C is a candidate for treatment, and the old practice of holding back until the liver showed damage has been abandoned. Treating early prevents fibrosis rather than chasing it, and it stops onward transmission. So the more useful question is not who qualifies but who is typically moved through quickly and who is asked to pause.

People with significant fibrosis or cirrhosis are generally prioritized, because every year of untreated infection adds risk of decompensation and liver cancer. People with hepatitis C alongside HIV, kidney disease or other liver conditions are also often seen promptly, as are those awaiting or recovering from organ transplantation. Anyone who continues to be at risk of passing the virus on, including people who inject drugs, is encouraged rather than deferred; drug use is not a reason to withhold treatment under any major guideline.

A short wait is usual in a few situations. Very recent infection is one: because a proportion of people clear the virus on their own within the first six months, some clinicians repeat the RNA test before committing to treatment, though others now treat acute infection directly. Pregnancy is another; treatment is generally deferred until after delivery, and the plan is made with the obstetric team. A newly discovered hepatitis B co-infection, a serious interacting medicine that cannot be changed safely, or advanced decompensated cirrhosis needing specialist assessment can all mean a pause while the picture is clarified.

A pause is not a refusal. If you are asked to wait, ask what specifically is being resolved and when you will be reviewed, and make sure a follow-up date is in the diary before you leave.

Hepatitis C pre-treatment tests at a glance

Seen together, the tests form a logical chain, each one narrowing the question until the treating team can choose a regimen with confidence. The table below sets them side by side.

Test	What it measures	What the result is used for	What it involves
Antibody test	Immune proteins made in response to the virus	Screening; shows past or present exposure	Blood draw
RNA (viral load) test	Presence and quantity of viral genetic material	Confirms active infection; baseline for later comparison	Blood draw, often same sample
Genotype test	Which strain and subtype of the virus is present	Guides choice and length of regimen where relevant	Blood draw; needs detectable RNA
Transient elastography	Liver stiffness as a proxy for scarring	Stages fibrosis from F0 to F4	Painless ultrasound-based scan, brief fast
APRI / FIB-4 scores	Fibrosis estimated from enzymes and platelets	Triage; rules advanced disease in or out	Calculated from routine bloods
Hepatitis B and HIV tests	Co-infections	Safety planning; avoids reactivation and interactions	Blood draw
Kidney and liver panels	Organ function and baseline values	Regimen suitability; monitoring reference	Blood draw
Medication review	All prescribed and non-prescribed products	Identifies interactions before starting	Conversation with pharmacist or clinician

Two patterns are worth noticing. Most of these tests can be drawn from one or two visits to the phlebotomy chair, so the list is longer than the experience. And only one of them, the fibrosis scan, tells you about your own health rather than about the virus or the medicines. If you remember a single number from this process, make it your fibrosis stage; it is the one that shapes what happens after the virus is gone.

What the following weeks usually look like

The stretch between a positive antibody letter and the first tablet is the part nobody warns you about, and it helps to know its shape.

The first week or two is usually about confirmation. The RNA test is run, sometimes on the original sample, and if it is positive the genotype is often requested from the same tube. Turnaround varies by laboratory, and it is reasonable to ask at the time of the draw when results are expected. A referral to a specialist, whether a hepatologist, an infectious disease physician or a trained nurse-led service, typically goes in around now.

The scan and safety bloods follow. Some services book elastography on the same day as the specialist appointment; others arrange it separately. Hepatitis B, HIV, kidney and liver results usually come back within days. The medication review happens at the consultation, and if an interaction is found, a letter may go to whoever prescribes the other medicine before the antiviral is confirmed.

Then treatment itself. The NHS describes a typical course of direct-acting antivirals as lasting eight to twelve weeks, taken as daily tablets, with longer courses reserved for particular situations such as cirrhosis or previous treatment. Blood tests during the course are often minimal; some services check a viral load partway through, while others simply check at the end.

The final milestone comes twelve weeks after the last dose, when an RNA test confirms whether the virus remains undetectable, the sustained virological response described earlier. WHO reports that pan-genotypic regimens achieve this in more than 95% of people treated. For those with cirrhosis, the story does not end there: liver cancer surveillance by ultrasound generally continues at regular intervals for life, because scarring that has already formed carries a risk of its own even after the virus has gone.

What people often get wrong about hepatitis C testing

Misunderstandings about these tests are common, partly because the terminology is dense and partly because much of what circulates online dates from the interferon era. A few corrections cover most of them.

“A positive antibody test means I have hepatitis C.” It means you have been exposed at some point. Roughly three in ten people clear the virus without treatment, according to WHO, and their antibody tests stay positive for life. Only the RNA test confirms active infection.

“A high viral load means my liver is badly damaged.” Viral load and fibrosis are independent. The scan and blood scores measure damage; the viral load measures how much virus is circulating that day, which fluctuates and does not predict outcome.

“Genotype 1 is the hard one.” That was true when interferon was the mainstay. With current direct-acting antivirals, all major genotypes respond well, and WHO’s figure of more than 95% clearance applies across them. Genotype now guides choice of regimen rather than predicting failure.

“My genotype could change to a worse one.” It cannot. The genotype is a fixed feature of the strain you acquired. A different genotype on a later test would indicate a new infection, not mutation.

“I feel fine, so my liver must be fine.” Fibrosis and even cirrhosis are silent for years. Feeling well is not a stage on the F0 to F4 scale, which is why the scan is not optional.

“Once treated, the antibody test will turn negative.” It will not. Successful treatment is confirmed by an undetectable RNA test twelve weeks after finishing. The antibody remains as a permanent marker of past infection and should not be used to check for reinfection.

“I need a biopsy to start treatment.” Most people do not. Non-invasive scans and scores have largely replaced biopsy, which is now reserved for unresolved questions.

Questions to ask your care team

A specialist appointment moves quickly, and the most useful questions are the ones you have thought about beforehand. These are the ones that tend to change what happens next.

• Is my RNA test positive, and what is my baseline viral load? Ask for the actual figures so you can compare them with later results.
• What is my genotype and subtype, and does it affect which regimen you are recommending or how long it runs? If genotype testing was not done, ask why it does not change the plan.
• What is my fibrosis stage, and how was it measured? Ask whether the scan result agrees with the blood scores, and if not, what will resolve the difference.
• Do I have cirrhosis? If yes, what monitoring will continue after the virus is cleared, and how often?
• Have I been tested for hepatitis B and HIV, and did anything come back that changes the plan?
• Which of my current medicines or supplements interact with the treatment, and who will manage any changes? Bring a written list rather than relying on memory.
• How long will the course last, and what check-ups happen during it?
• When will the final blood test be done, and how will I be told the result?
• What should I do if I miss a dose or am unwell during treatment? Get the clinic’s contact route before you start.
• Can I be reinfected, and how would that be detected?

Write down the answers, or ask whether a summary letter will be sent. Several of these numbers, especially the fibrosis stage and baseline viral load, are worth keeping in your own records, because they form the reference point for everything that follows. If something is unclear, say so during the appointment; a good team would rather explain twice than have you leave uncertain about your own results.

When to call your doctor

Most of the testing phase is uneventful, and the medicines that follow are generally well tolerated. Still, a few signs warrant a same-day call to your clinic or, out of hours, urgent care, whether they appear before, during or after treatment.

Seek urgent help if you notice yellowing of the skin or the whites of the eyes, unusually dark urine together with pale stools, or itching that is severe and unexplained. These can indicate that the liver is struggling, and in someone with known scarring they should not be watched at home. The same applies to vomiting blood or material that looks like coffee grounds, passing black or tarry stools, or a rapidly swelling abdomen; each can signal bleeding or fluid build-up linked to advanced liver disease and needs emergency assessment.

New confusion, unusual drowsiness or a marked change in personality in someone with cirrhosis can reflect a build-up of toxins the liver would normally clear, and should be treated as an emergency by whoever is with them. Severe pain in the upper right abdomen, a high fever, or easy bruising and bleeding from the gums also merit prompt review.

During treatment, contact the clinic rather than stopping tablets on your own if you develop a rash, persistent nausea, or symptoms of a hepatitis B flare such as fatigue with dark urine. Never adjust or stop antivirals without speaking to the prescribing team; an incomplete course reduces the chance of clearing the virus and can allow resistance to develop.

For non-urgent worries, including results you do not understand or a follow-up appointment that has not materialized, a call to the clinic or your primary care office is the right step. The people who ordered these tests expect questions about them.

Frequently asked questions

What is the hepatitis C viral load meaning on my lab report?

Viral load is the amount of hepatitis C genetic material in a set volume of blood, reported in international units per milliliter. A detectable result confirms active infection. The size of the number does not reflect how damaged your liver is or how likely treatment is to work; it serves as a baseline so that later tests can show whether the virus has become undetectable.

Hepatitis C antibody vs RNA test: why did I need both?

The antibody test detects the immune system’s response and stays positive for life after any exposure, so it cannot tell a current infection from one your body cleared years ago. The RNA test looks for the virus itself and confirms whether infection is active now. Clinics run the antibody test first as a screen and the RNA test second to confirm, often on the same blood sample.

Is a liver fibrosis scan for hepatitis C painful or risky?

No. Transient elastography uses a probe on the skin over the right ribs that delivers gentle mechanical pulses, felt as light flicks, while ultrasound tracks how fast the wave travels through the liver. There is no radiation and no needle, and the scan takes a few minutes. You may be asked to avoid eating for a few hours beforehand because a recent meal can raise the reading.

HCV genotype 1a vs 1b: does the subtype change my treatment?

Both are subtypes of genotype 1, the most common type in the United States. With current direct-acting antivirals, both respond well, and many regimens cover them identically. The subtype can matter in specific situations, such as deciding whether to check for resistance mutations before certain regimens, or when planning a second course after an earlier one did not clear the virus. Your prescribing team will say whether it affects your plan.

Can my hepatitis C genotype change over time?

No. The genotype is a permanent characteristic of the strain you acquired at infection, and it does not mutate into another genotype. If a later test shows a different genotype, that indicates a new infection with a different strain rather than a change in the original virus. This is one reason people who remain at risk are advised to have repeat RNA testing after successful treatment.

Do I need a genotype test if the treatment works against all genotypes?

Not always. WHO recommends pan-genotypic regimens partly so that treatment can start without genotyping where testing is slow or unavailable, and some programs have removed it from the routine pathway for people without cirrhosis. Many specialist services still order it because the result can open genotype-specific options, guide resistance testing, and help interpret outcomes. Either approach is guideline-supported; ask your team which applies to you.

What does an F0 to F4 fibrosis stage mean?

It is a scale of liver scarring. F0 means no fibrosis, F1 and F2 mild to moderate scarring, F3 advanced fibrosis, and F4 cirrhosis, where scar tissue has changed the liver’s structure. The stage is estimated from stiffness on elastography, from blood scores, or occasionally from biopsy. It influences treatment length in some cases and determines whether long-term monitoring is needed after the virus is cleared.

Why was I tested for hepatitis B before hepatitis C treatment?

Because clearing hepatitis C with direct-acting antivirals can, in some people who carry a dormant hepatitis B infection, allow that second virus to reactivate and inflame the liver. Prescribing information for these medicines carries a formal warning about this, and CDC guidance recommends checking hepatitis B status first. If hepatitis B is found, the treating team plans monitoring or treatment for it alongside the hepatitis C course.

How long after treatment is the final hepatitis C blood test?

The confirmatory RNA test is done 12 weeks after the last dose, according to NHS guidance. An undetectable result at that point is called a sustained virological response and indicates the virus has been cleared. The antibody test is not used for this purpose because it stays positive permanently. People who remain at risk of new exposure may be offered periodic RNA tests afterwards.

Will my viral load tell me if the treatment is working partway through?

Some services check a viral load during the course to confirm the virus is falling, while others rely on the end-of-treatment and 12-week tests alone; both approaches are accepted. A partway result showing a large drop is encouraging but does not by itself confirm clearance. The definitive answer comes from the RNA test 12 weeks after finishing, which your team will schedule.

References

• CDC: Testing for Hepatitis C
• CDC: Clinical Overview of Hepatitis C
• World Health Organization: Hepatitis C fact sheet
• NHS: Hepatitis C: Diagnosis

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.