Liver specialists, virologists and immunologists from around the world met at the 3rd International Workshop on a Hepatitis B Cure in Toronto last week to share their advances and brainstorm solutions to the challenges they face as they hunt for a cure for the liver infection that affects 240 million worldwide.
Eradicating hepatitis B virus (HBV) infection is no easy task. HBV is a far more complicated and resilient virus than hepatitis C, and scientists predict a cure will require a careful orchestration of drugs and immune-enhancing treatments that could:
Eliminate HBV antigens—especially the hepatitis B surface antigen (HBsAg). This viral protein appears able to “exhaust” or disable the immune system’s T cells so they’re unable to effectively fight the infection.
Find a vulnerability in the HBV replication cycle that can be exploited to keep the virus from entering liver cells and inserting its genetic material (cccDNA) required for viral reproduction.
Enhance or “wake up” the exhausted T cells, after HBsAg is reduced or eliminated, so the immune system can successfully eradicate the HBV-infected liver cells.
As researchers learn more about why HBV is so successful at evading the immune system and hijacking liver cells for viral production, they are also realizing how much they don’t know and what tools they lack to identify if and when they find successful treatment strategies. Here are some of the challenges the researchers addressed during the day-long brainstorming session.
What will a cure look like? Can scientists ever expect to totally eradicate HBV from the liver? Even when healthy adults are able to clear HBV following an acute infection, small reservoirs of the virus remain – similar to chicken pox that causes shingles later in life when the immune system can no longer hold it in check. Should researchers instead set their sights on a cure that duplicates what Mother Nature now achieves following an acute infection, which simply eradicates most of the virus and greatly reduces the risk of liver damage.
Do researchers currently have the right tools to identify when a treatment works? Nearly all hepatitis B lab tests used today evolved from blood bank tests designed to identify HBV-infected donated blood. As a result, lab tests produce a “positive” or “negative” measurements for the presence of antigens and antibodies, but nothing more nuanced. Labs measure the amount of HBV DNA (viral load) in a patient, but rarely measure HBsAg even though patients can have an undetectable viral load and still have lots of HBsAg circulating in their bodies.
But figuring out when a treatment is able to reduce HBsAg or other antigens may be critical to a cure. Several research initiatives are working to reduce HBsAg, which is produced in great quantities and is believed to prevent the immune system from actively attacking the infection. But right now, most lab tests in the U.S. don’t measure how much HBsAg a patient has in their bloodstream.
“We don’t have great assays (lab tests) for measuring treatment responses (to current or new drugs),” said workshop panelist Jordan Feld, a clinical scientists and researcher from the Toronto Western Hospital Liver Center.
“Maybe we don’t have the right endpoints to measure how effective treatment is,” said Marion Peters, chief of hepatology research at the University of California at San Francisco. “A treatment might be having an effect, but we don’t know what to measure so we don’t know it.”
A lost research opportunity with TAF clinical trials? On Nov. 10, the U.S. Food and Drug Administration (FDA) approved TAF, a new, lower-dose formulation of tenofovir that channels the antiviral more effectively to infected liver cells while reducing the drug’s impact on kidney function and bone loss. Because TAF’s clinical trials focused primarily on comparing the reformulated drug’s impact on viral load, ALT (liver health) and side effects, researchers did not conduct liver biopsies on TAF clinical trial participants.
While lower-dose TAF was found to work as well as tenofovir in slowing viral replication, it did something that researchers didn’t expect. During one clinical trial, 50 percent of patients treated with TAF achieved normal ALT levels–indicating no liver damage– compared to only 32 percent of patients treated with tenofovir.
Why was TAF so effective on liver cells? Was it able to remove some of the cccDNA or prevent HBV from replicating in liver cells in a way that tenofovir could not? “There seems to be a correlation, but because they didn’t have that possible endpoint in mind, they didn’t think to perform liver biopsies, which would have answered some of those questions,” Dr. Peters commented.
“We need to go beyond commercially-available tests so we can see with better sensitivity whether TAF or another drug would actually be more efficient and see what the effect is within the liver,” observed Fabien Zoulim, MD, PhD, associate director of the Liver Department at the Hôtel Dieu hospital in Lyon (France) and scientific director of the INSERM Unit 871.
How to eliminate HBV-infected liver cells without damaging the liver: In chronic hepatitis B, a large percentage of liver cells are infected. Some treatments in development, such as those using small interfering RNAs technology, target HBV antigens including HBsAg and quickly reduce their numbers. Using a combination treatment of antivirals to reduce viral load and RNAii technology to eradicate HBsAg, the immune system can swing into action and attack the infected liver cells. But how do you pace this “attack” so the liver is not severely damaged and the patient’s health threatened?
If only a small percentage of infected liver cells are killed during treatment, others will survive and continue to churn out virus. Kill too few infected liver cells and continual re-treatment is required. Kill too many liver cells and a patient could die from liver failure.
Flares are inevitable when the immune system is attacking infected liver cells – such as during an acute hepatitis B infection — but can this clearance be controlled without harming the patient?
The day before the workshop, the FDA ordered Arrowhead Pharmaceuticals to stop its Phase II human trials of its ARC 520 drug that uses RNAii to eradicate HBsAg after reports of deaths in animals that had been given high doses of the drug. The doses were much higher than were administered to humans in the Phase II clinical trial, which was evaluating the reduction of HBsAg after intravenous administration of ARC-520 in combination with entecavir or tenofovir. Panelists noted that this potential cure may still have promise, but the treatment dose must be examined and monitored carefully.
The workshop presentations highlighted the inevitable setbacks and advances that scientists make in the search for a cure. But optimism remained. Never have so many researchers been working from so many directions to find the synergistic solution that will one day reduce HBsAg, stop HBV from reproducing and spur T cells to attack infected liver cells.
One panelist suggested in the next five years, researchers should be able to develop ways to reduce viral load while enhancing the immune system’s T cell response to eradicate a hepatitis B infection. Around the world, 240 million people living with hepatitis B are waiting anxiously.
The Hepatitis B Foundation was a partner of the workshop. For more information about the workshop and researchers’ presentations, please click here.
With the cost of healthcare and prescription drugs soaring, it’s important for people age 65 and older who live with hepatitis B to shop for Medicare coverage carefully before they sign up by Dec. 7, especially if they need costly antivirals and frequent lab tests.
As we age, our immune system weakens and loses its ability to suppress our hepatitis B infection. We may notice a gradual rise in our viral load (HBV DNA) and/or our liver enzymes (ALT/SGPT), which indicate liver damage.
We may also experience other medical conditions, such as cancer or arthritis that require immune-suppressing drugs that unfortunately enable our hepatitis B to reactivate. To lower our viral load and reduce the risk of liver damage, we’ll need antivirals, and they’re not cheap. Medicare recipients must shop carefully for the most affordable plan. Here are the three key Medicare coverage areas:
Part A is free. It covers most of hospital and nursing home care, however you still pay for some deductibles and copays. For example, if you go to a hospital for a liver biopsy, you will pay a portion of that cost if you only have Part A.
Part B covers doctor visits and lab tests, and it costs about $150 a month and increases based on your income. There is a deductible of $166 a year and you pay a 20 percent copay for many services. Instead of selecting Part B, you may instead choose a private or employer-sponsored Medicare advantage plan.
Part D covers your drug costs and it’s optional, but if you’re on antivirals, interferon or other medications, it important that you have drug coverage under this or a Medicare Advantage plan (such as HMOs or PPOs) that cover all Medicare benefits including drugs. If you have a low income, you may be eligible for assistance to help pay for your Part D plan.
It is critical that you shop around before selecting a drug plan. Just like the Affordable Care Act’s Health Exchange, there will be fewer drug programs available to you to choose from this fall. You also need to make sure your plan:
Has your specialist or primary care doctor and lab in its network, and
Offers the lowest copay for the drugs you need.
When you shop for a Medicare Part D drug plan: You select from plans based on where you live and what drugs you take. For example, if you’re shopping for a drug plan to cover tenofovir (Viread), plan prices can vary by more than $1,000 a year. Comparison shopping is critical!
To find a plan, go to Medicare Plan Finder and enter your zip code and select the drugs you expect to take during 2017. It’s a good idea to sit down with someone who can help you during your search or call a Medicare representative at 1-800-633-4227 (1-800-MEDICARE) as you search online.
The drug plans have different pricing tiers for prescription drugs, a simple generic antibiotic can be less expensive Tier 1 or 2 drug, while a brand name drug like tenofovir can be a more costly Tier 4 or 5 drug. Without Part D drug coverage, a year’s supply of tenofovir could cost about $12,880 a year. Before you select a plan, here are some suggestions:
Check the fine print: Make a list of all of your medications and check how much each plan reimburses for each. Search for any “hidden extras” you’ll have to pay if you’re using a brand name or specialty drug. Some plans have separate, high copays for brand-name and specialty drugs, which can include hepatitis B drugs.
If you need a brand-name maintenance drug (like tenofovir) that isn’t available as a generic yet, you may want to focus only on plans that have the lowest co-pay for that drug. Your other drug needs may be less expensive, generic cholesterol- or blood pressuring-lowering medication.
Consider both the monthly premium and the copay. You must consider both costs when searching for the best plan.
Does the plan require you to use a specific pharmacy? An increasing number of plans require you to use a preferred pharmacy, or even a mail-order option. Factor in convenience and your premium and copay.
Can you get discounts because of your income? You may be eligible to get all or part of your Medicare premiums, deductibles or co-payments covered if you have limited income and resources. Individuals with incomes less than $17,820 and assets less than $13,640, and couples with incomes less than $24,030 and assets less than $27,250, qualify for subsidies. You also may qualify, even if your income is higher, if you support other family members who live with you. Call Social Security at 800-772-1213 for information.
The good news: The dreaded “doughnut hole” or the gap during which you must pay a higher percentage of your drug costs, continues to shrink next year and will be completely phased out in 2020.
Even if you’re happy with what you had last year, do your research: Kaiser Foundation research found only 10 percent of Medicare enrollees switched plans between 2007 and 2014. Those who switched on average saved about $16 a month just on premiums. It pays to shop around.
Like your doctor? Make sure he/she is in your provider networks: Advantage plans can shuffle their provider and hospital networks each year. And their provider lists may not be included in Medicare’s online Plan Finder or the basic plan documents.
Contact your plan and ask for their 2017 provider directory before making a decision. Check if specialty facilities like university-based teaching medical centers are included. Or, call your physician and ask if they will be in the plan you’re considering — and, if not, where they’re going. And be aware: While doctors can leave a plan in the middle of a year, you typically can’t.
For more than 25 years, Timothy Block, Ph.D,, has worked tirelessly to find a cure for hepatitis B, promoting research, writing papers, mentoring students and collaborating with experts around the world to find a cure for the 240 million people living with this deadly liver disease.
Today, the cofounder and president of the Hepatitis B Foundation, the Baruch S. Blumberg Institute and the Pennsylvania Biotechnology Center, is optimistic and believes there are new therapies in sight for those living with chronic hepatitis B.
An unprecedented number of researchers are scrutinizing every stage of the hepatitis B virus (HBV) replication cycle to find its vulnerabilities and develop drugs to permanently disable it. The cure Block wants would completely eradicate the infection so no one would ever wake up worrying about the risk of liver damage or cancer to themselves or a loved one.
This global, active march towards a cure is in stark contrast to 1991 when Block began his solitary quest, after a friend’s devastating hepatitis B infection made him rethink his career and start focusing on the liver disease that infects more than one in three people worldwide.
Twenty-five years ago, the only available treatment was conventional interferon, which was largely ineffective. The first antiviral, lamivudine, appeared shortly thereafter. It would be one of several to emerge from HIV’s drug arsenal. Since then, more antivirals designed to disrupt HBV’s replication process have been developed that target the polymerase—the essential enzyme needed for HBV replication.
“But they are not cures,” Block explained during a recent webinar. “They’re good at reducing viral load (HBV DNA), but they don’t get rid of the virus, and considerable viral DNA and hepatitis B surface antigen (HBsAg) remain in liver cells.” Nor do current antivirals get rid of the HBV chromosome called cccDNA that embed in liver cells and stubbornly remain, ready to churn out more virus if a person stops taking antiviral drugs, or if their immune system weakens due to advancing age or another illness.
There are other roadblocks that make hepatitis B far harder to cure than hepatitis C. HBV generates massive amounts of HBsAg that appear to overwhelm the immune system’s B cells, whose job is to produce antibodies to eradicate HBV’s antigens. When newborns or young children are infected, these B-cells become paralyzed or “exhausted” by the flood of HBsAg engulfing them and they don’t generate the antibodies needed to fight infection. In contrast, when healthy adults are infected, these B-cells act quickly and aggressively to eradicate HBsAg within six months.
“Now for the first time, we’re looking beyond the polymerase to find more targets that are essential for HBV replication,” Block explained. HIV researchers have already done this and have identified more than 30 different “targets” in the HIV replication process. Hepatitis B researchers are also expanding their target range.
There are now new drugs in development, some have even reached Phase II clinical trials, that target new HBV reproductive terrain. They employ a variety of strategies ranging from immune system enhancers to molecular weapons designed to halt cccDNA integration into liver cells.
“If you can suppress cccDNA, the game would be over,” Block said, “but cccDNA is small, tough target. It’s so small compared to other material, that it’s almost impossible to distinguish from other molecules.” However, biologicals that are able to “inhibit” or block cccDNA from entering a liver cell could stop the virus from hijacking and reproducing in liver cells. Here are some types of drug strategies currently in development that could lead to a cure:
Restructured versions oftenofovir: There are two new tenofovir “prodrug” compounds, called TAF and CMX 157, that are more effective at reaching liver cells and impeding HBV replication. TAF is now in Phase III clinical trials and is expected to reach the U.S. Food and Drug Administration (FDA) this month (November 2016).
Molecular agents that target and disable HBV replication:
A new agent, called the CRISPR/Cas9 system, may be able to operate on a molecular level to search out and destroy HBV cccDNA molecules.
One of the more advanced molecular strategies, already in Phase II trials, is a “silencing” RNA process. This approach uses RNAi gene silencers to target and destroy HBV RNA to prevent viral reproduction. “CccDNA remains,” Block explained, “but all of its gene products it needs are choked.”
Entry inhibitors: Some of these drugs resemble HBsAg, but they work as decoys to prevent the virus from entering or binding to the liver cell. One is in Phase II clinical trial.
Capsid inhibitors: This approach interferes with the viral DNA’s ability to connect or glue together during the replication process. Several of these drugs are in Phase II clinical trials.
HBsAg inhibition and eradication: “There are 1 million more HBsAg as the actual virus,” Block observed. “Why are there so many? What is it doing in the blood? Why is it able to exhaust our B-cells?” Because HBsAg appears to hold a key in stopping infection, researchers are working to develop a way to eradicate HBsAg. Two of these HBsAg eradicator products are in Phase II trials.
Adaptive and innate host defense: This approach involves a two-step strategy, first reducing viral load to undetectable levels by helping liver cells become “in-hospitable” hosts to HBV’s reproductive efforts, and then introducing a vaccine or some other immune enhancer that can break the B-cell exhaustion cycle while firing up immune cells to aggressively fight and eradicate the infection. There are several of these drugs in Phase I and II clinical trials.
Block told his webinar audience that ideally one of these drugs would emerge as a single, simple cure. “But every infectious disease today, such as hepatitis C and HIV, is almost always treated with a combination of drugs. We might see two direct-acting antivirals and maybe a third drug that work as an immune system activator.”
When asked which patients would get first access to a new cure, Block predicted that people with high viral loads and liver damage would be treated first based on medical need. “As drugs get safer, I hope we will treat people in the immune tolerant phase (with high viral load but no signs of liver damage yet), before they begin to have signs of liver damage.”
Your daily antiviral pill can save your life when you have liver damage from chronic hepatitis B. Entecavir or tenofovir (Viread) quickly reduce the amount of virus in your liver and the damage it causes.
All you have to do is take it. Every day. But 20 to 30 percent of prescriptions are never filled, and about 50 to 70 percent of us don’t take our medications as prescribed. When we stop taking our daily antiviral, hepatitis B can reactivate and threaten our health.
In one study, researchers provided 100 hepatitis B patients with an entecavir pill dispenser that monitored whether or not they took their daily pill over a 16-week period. They found about 70 percent of patients took their antiviral pill as prescribed more than 80 percent of the time — which means these patients were “medication compliant.”
Those who missed taking their antivirals more than 20 percent of the time–and were “noncompliant”–tended to be younger and had indifferent attitudes about whether or not the antiviral was really needed or would work.
According to experts, whether we are “medication compliant” or not depends on how much trust we have in our doctors. If we like our healthcare provider and feel comfortable asking questions, we’re much more likely to take our medication on time. And, if our friends and family support and encourage us, we’re even more inclined to take our medication as prescribed.
“The trust I have in my doctor is a big factor,” said a member of the Hepatitis B Support List. “It is important to find a doctor who understands hepatitis B and is willing to work with me in terms of explaining what the options are and what the best approach is in managing my condition.”
Medicare insurance pays for seniors to get vaccinated against hepatitis B, but it doesn’t cover testing to find out if they’re infected and need life-saving treatment. The federal government is now poised to close this glaring healthcare gap that prevents at-risk seniors from getting screened for hepatitis B.
Currently, the majority of the estimated 2 million Americans with chronic hepatitis B are over age 50, and the longer they are infected, the higher their risk of liver damage and cancer. This preventive screening saves lives and is cost-effective, because treatment with antivirals quickly and effectively reduce liver damage.
Until the Hepatitis B Foundation, Hep B United, the Association of Asian Pacific Community Health Organizations and the National Viral Hepatitis Roundtable asked the federal government to cover screening, seniors who wanted to be tested for hepatitis B had to pay for the test themselves. Because hepatitis B is a “silent” infection, causing few symptoms until cirrhosis or cancer develop, nearly two-thirds of Americans living with hepatitis B have never been tested, identified or referred to life-saving treatment.
The highest rate of liver cancer in this country is in Vietnamese-American men, many of whom were never tested for hepatitis B. By the time they are diagnosed, it is often too late. Here’s two more examples of the high cost of this healthcare gap:
The Charles B. Wang Community Health Center in New York City serves a large Asian-American population. When the clinic screened all of its patients for hepatitis B, it found 7.8 percent of patients age 65 and older were chronically infected and 45 percent had been infected in the past.
Another New York City study of African immigrants, which included all ages, found 9.6 percent of them were chronically infected.
Today, the most vulnerable Americans are infected at a rate 10-times the national average, yet until now the government didn’t cover the cost of screening them. Medicare did cover testing if there were signs of liver damage from other medical tests, but in the case of late-stage hepatitis B infections, a diagnosis often comes too late for treatment.
Screening seniors for hepatitis B has a life-saving ripple effect across generations. When hepatitis B is diagnosed in a grandparent, there is an opportunity to educate, test and vaccinate their children and grandchildren who are also at risk.
Under the new guidelines, which also apply to disabled people covered by Medicare Part B, Medicare will reimburse primary care providers when they screen people at risk of hepatitis B, including:
People born in regions with high hepatitis B rates, including Asia, Africa, the Middle East, the Caribbean, Eastern Europe, and some areas of South and Central America.
Second-generation residents who were not vaccinated at birth and whose parents come from high-risk regions, such as sub-Saharan Africa and central and Southeast Asia
HIV-positive persons, injecting drug users, men who have sex with men, and
Family and household members of people with chronic hepatitis B.
This expanded coverage will go far to screen seniors, but gaps remain.
Under the proposed guidelines, only primary care providers can order testing, but many specialists including oncologists, rheumatologists and gastroenterologists see patients at risk for hepatitis B. The expanded coverage should include them and also pharmacists.
Additionally, both providers and the public need to know more about hepatitis B. Today, the majority of people infected with hepatitis B don’t know they’re infected. Patients often don’t share their true stories of activities that may put them at risk of hepatitis B, especially if it includes sexual abuse or injecting drug use, and doctors often don’t have the time or the skills to elicit this vital information. Along with expanded coverage should come public education to provide a common language for these difficult conversations.
Lastly, while providers are screening more Asian-Americans for hepatitis B, many of those at-risk remain undiagnosed, including first- and second-generation African immigrants.
This expanded Medicare coverage is long over-due, but we have a long way to go.
To read the proposed, expanded coverage for hepatitis B testing, please click here.
To submit a comment about the proposed coverage, click here .
How far are we from finding a cure for hepatitis B? We are close, said Timothy Block, PhD, president and co-founder of the Hepatitis B Foundation and its research arm, the Baruch S. Blumberg Institute. He points out that hepatitis C, once thought to be incurable, is today cured with new combination treatments.
Experts believe a cure for hepatitis B will also soon be developed. And the need for a cure has never been greater, with more than 240 million people worldwide living with chronic hepatitis B, causing 1 million deaths per year from related liver failure and liver cancer.
“Treatments are available,” explained Block, “but we have become a little too comfortable with the medications that are currently approved for use.” While these drugs are effective, interferon has many side effects and daily antivirals require lifelong use. These drugs work in only half of the infected population and reduce death rates by only about 40 to 70 percent.
What will a cure look like?
The available antivirals are similar and combining them offers no advantage. They have limited effectiveness against cccDNA, the seemingly indestructible “mini-chromosome” of the hepatitis B virus that continues to produce virus particles in infected liver cells, even in people being treated. A cure, therefore, would have to destroy or silence cccDNA and provide long-term immunity. Because one-drug treatments can lead to drug resistance, a cure would almost certainly involve combination therapy, similar to hepatitis C. Continue reading "Is a Cure for Hepatitis B Coming? Experts Say Yes"→
The majority of people infected with hepatitis B lead healthy and normal lives. However, a small number of people may develop liver disease that will dramatically affect their quality of life and their ability to work on a short-term or long-term basis.
They may not be able to work for several weeks because of side effects from pegylated interferon treatment, or progressive liver damage could make it impossible to work and support themselves and their families even after treatment.
For years, people with pre-existing conditions like chronic hepatitis B struggled to get health insurance. News stories and Michael Moore’s documentary Sicko highlighted insurance companies’ refusal to cover pre-existing conditions and their practice of inflating premium prices if consumers had chronic health problems.
Outraged by industry efforts to cover only low-cost, “healthy” consumers, lawmakers banned discrimination against pre-existing conditions in the Affordable Care Act (ACA – Obamacare). The ACA’s Healthcare Marketplace website promises, “Your insurance company can’t turn you down or charge you more because of your pre-existing health or medical condition like asthma, back pain, diabetes, or cancer.”
To prevent liver damage and cirrhosis and reduce the risk of liver cancer–especially in older patients who’ve had hepatitis B for decades–doctors often prescribe long-term antiviral treatment. But some antivirals cause minor bone loss, which poses a problem for older patients with osteoporosis.
According to experts, the risk of bone loss from long-term antiviral treatment is low, and in fact some antivirals do not cause any bone loss at all. But if you are starting antivirals at an older age, or if you have been on antivirals long-term, experts recommend you monitor your potassium and vitamin D levels and regularly test for bone loss in the hip area so you know if you are experiencing bone loss and need a calcium or vitamin D supplement. Continue reading "Taking Antivirals Long-Term for Hepatitis B? Should You Worry About Bone Loss?"→
If you have been diagnosed with chronic hepatitis B, your doctor has probably run several blood tests that show if the infection is harming your liver and identify what stage of infection you are in. Doctors consider all of these results when deciding if you need treatment and how often you should be monitored.
In this blog, we’ll examine how one of the tests — the HBV DNA or viral load test –can give you a snapshot into your hepatitis B infection and your health. The HBV DNA test is performed on a blood sample using a Polymerase Chain Reaction (PCR) technique that rapidly generates HBV DNA fragments so they can be measured. Today, viral load is usually measured using international units per milliliter (IU/mL). However, in the past it was measured in copies per milliliter (copies/mL), and in some regions and labs, it is still used.
If you ever need to convert copies into international units, there are about 5.6 copies in one international unit, so 5,000 copies/mL equals about 893 IU/mL. Remember to keep copies of your lab information on file so you can track your status. An Excel spreadsheet works great.
The sensitivity of HBV DNA tests may vary with each lab so it’s a good idea to always use the same lab for your test. Labs usually measure down to about 300 IU/mL. Below that threshold, the viral load is considered “undetectable” – something all of us with chronic hepatitis B wants to hear.
How HBV DNA results are presented mathematically on your lab report can be confusing. Because the amount of virus in the blood may be very high – in the millions or billions – the result may be displayed as an exponent or a log, rather than a whole number. If this is confusing to you, please take a look at this explanation on the math.
What does viral load say about what stage of hepatitis B you are in? Your viral load also varies over time, depending on your age and “stage” of infection.
Children and adults in the “immune tolerant” stage can have viral loads in the millions or even billions. It sounds scary, but it’s not unusual. Your viral load can remain very high for decades until your immune system begins attacking the infection. Most children and young adults who test positive for the hepatitis B “e” antigen (HBeAg) generally have high viral loads, generally doctors don’t treat patients in this stage. Once their immune systems get rid of HBeAg and generate “e” antibodies (HBeAb), their viral loads begin to decline.
Adults with undetectable or low viral loads and no signs of liver damage are in an “inactive” stage. Adults with normal ALT (SGPT) levels, which indicate no current liver damage, and undetectable or viral loads less than 2,000 IU/mL generally do not require treatment.
People in the “active” stage with elevated viral loads and signs of liver damage need treatment. Many people in their 40s, 50s or 60s, develop HBeAg-negative hepatitis B. Though individuals may have lost HBeAg, the virus has mutated over time and is able to keep replicating, putting these older patients at risk of liver damage. Doctors recommend antiviral treatment if these patients’ viral load exceeds 2,000 IU/ML and their ALT levels are elevated.
Why is it important to measure HBV DNA during treatment? When daily antiviral pills (either tenofovir or entecavir) are prescribed, doctors measure your HBV DNA to see if the drug is working to reduce your viral load. Antivirals work by meddling with the viral DNA so the virus cannot reproduce effectively. Doctors measure your viral load to make sure the antiviral is working.
Why is measuring viral load important if you’re pregnant? Today, all pregnant women are screened for hepatitis B, and experts also want their viral loads to be measured. When pregnant women have high viral loads—exceeding 200,000 IU/mL—medical guidelines recommend antiviral therapy during their third trimester of pregnancy to reduce their risk of infecting their newborns. Babies born to HBV-infected women can become infected even if they are immunized at birth and treated with HBIG (hepatitis B antibodies) if their mothers have high viral loads.
It is important to remember that a viral load test provides you with important information, but it must be considered in relation to your other HBV and liver function tests results to determine if treatment is needed at all, or if you are responding favorably to current treatment. Although an undetectable or low viral load is good news, it does not necessarily guarantee that you have not, or will not experience liver damage. Hepatitis B is a tricky virus. Talk to your liver specialist about all of your test results.