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HIV/HCV Coinfection: Clinical and Research Challenges
Baltimore, Maryland Oct 11th – 12th, 2001


“Today if you are not confused, you are just not thinking clearly” HIV Researcher

On Thursday, October 11, 2001, the Forum for Collaborative HIV Research and Division of AIDS, National Institutes of Allergy and Infectious Diseases and the NIH sponsored the first ever conference on HIV/HCV Coinfection in Baltimore, Maryland. This two-day conference brought together experts in HIV, HCV, HIV/HCV coinfection, HIV/HBV and liver transplantation in HIV patients. The experts included physicians who have undergone research in these areas, public health officials and community activists in both HIV and HCV.

The first day of the conference consisted of fifteen sessions on clinical data presented by researchers, physicians, public health experts and community activists. On the second day the groups broke out into eleven working groups to brainstorm and make recommendations for future research on various components of HIV/HCV coinfection.

Day One

Opening Session

The opening session was a welcome by June Bray from the Forum for Collaborative HIV Research, who moderated the entire day and Dr. David Thomas from Johns Hopkins University, Department of Infectious Diseases. During the opening comments Dr. Thomas discussed how opportunistic infections have declined due to the introduction of protease inhibitors between 1996 to 1999 but during that same period the incidence of end stage liver disease (ESLD) in HIV patients has increased considerably. This is due in large part to HCV infection in the HIV population. He estimated that 200,000 patients in the U.S. are currently infected with HIV/HCV coinfection, which is 20-30% of the total HIV infected individuals. The majority of the cases come from IDU’s and to a lesser extent from sexual transmission. Dr. Thomas posed some very interesting questions.

  • What is the frequency of false negative Antibody HCV in HIV/HCV coinfected individuals
  • Liver biopsy – should it be routinely done in patients with HIV?
  • Does HIV/HCV coinfection from injection drug use (IDU) impact ESLD?
  • Does HCV accelerate progression of HIV? The reason that this question is being asked is because it is believed that HIV accelerates HCV progression.
  • HIV patients on highly active antiretroviral therapy (HAART) therapy get a CD4 lymphocyte restoration. Is this phenomena impaired in patients with HIV/HCV coinfection?
  • How does antiretroviral therapy (ART) impact liver toxicity in a patient that is HIV/HCV coinfected?
  • How does HIV/HCV coinfection impact mitochondrial toxicity and lactic acidosis?

During the opening remarks Dr. Marion Peters from UCSF was asked to say a few words. She said that there are important clinical care issues that need to be addressed as well as important research in the area of HIV/HCV coinfection that needs to be done. She also stated that it was important to think what questions need to be answered in the next five years in HIV/HCV coinfection and that it is time to think outside the box - no idea could be considered crazy!

Session One: The Challenges in a Research Agenda for HIV/HCV Coinfection
Dr. Edmund Tramont from NIAID-NIH Division of AIDS

Dr. Tramont opened his session by stating that the bug or the virus is similar in both the HCV and the HIV/HCV coinfection populations. It is the clinical disease course of the infection that is different. This difference is due to the host immunologic response to the disease.

Dr. Tramont then listed the known facts of HIV/HCV coinfection:

  • Coinfection is common
  • Higher HCV-RNA levels in the coinfected patients versus the HCV monoinfected patient
  • Higher rate of hepatotoxicity associated with antiretroviral therapy (ART)
  • Comparable treatment results with combination therapy in HCV and HIV/HCV coinfected patients
  • In HCV the patient’s cell mediated response is directly related to outcome. In a HIV/HCV coinfected patient there is not a broad and strong cellular immune response and it is thought that this is related to the faster progression of HCV.
  • In the era of HAART morbidity and mortality due to associated with complications of ESLD is a growing problem
  • ESLD is the leading cause of death in HIV patients

Dr. Tramont then discussed the challenges and opportunities in HIV/HCV:

  • To determine the immunological defect responsible for the blunted cellular immune response to HCV in HIV/HCV coinfected patients
  • Need more therapeutic options for the treatment of HCV
  • Determine mechanism causing the defect that leads to an increase in hepatotoxicity in antiretroviral drugs so that drug therapy can be better managed. He also stated that we need to manipulate current drugs pharmacologics to decrease toxicity.

A comment was made by Jules Levin of NATAP, a patient advocate that the NIH, Federal Government, VA and NIDDK has to date done a poor job to address HIV/HCV coinfection. Mr. Levin also commented that much more needs to be done and the bureaucracy doesn’t respond rapidly enough to address the current needs of this community. Mr. Levin stated that the ACTG has been the only agency responsible in trying to deal with HIV/HCV coinfection and that Dr. Marion Peters who is heading up the LD Focus Group should be commended for her commitment. Dr. Tramont responded by agreeing that bureaucracy is extremely slow to respond and that unfortunately too many people will have been negatively impacted by the time change occurs. He stated that they are using a Matrix Management model to get a global approach to managing HIV/HCV but it’s been slow to get divisions to collaborate together.

Session Two: The Epidemiology of Hepatitis C Virus and HIV Coinfection
Dr. William Bower, Division of Viral Hepatitis for the CDC

Dr. Bower started his talk by going over the epidemiology of HIV/HCV coinfection. He stated that there are overlapping routes of transmission. He also stated that there are high levels of coinfection in the U.S and that there are significant implications for care of these patients. He quoted “there are 3.9 million patients infected with HCV in the U.S and 800,000 infected with HIV.” He discussed factors that promote progression of HCV including:

  • Increased alcohol intake
  • Age over 40 years at time of infection
  • HIV coinfection
  • Others but not thought to be as significant
  • Male gender
  • Coinfection with HBV or other viruses

Next Dr. Bower went onto discuss prevalence data by population in the United States. He stated that of all the HCV cases in the United States, 60% were among whites, 20% among blacks, 7% among Mexican-Americans and 2.9% among other populations. Furthermore, he stated that in both males and females the prevalence peak is between 40 and 59 years and that during this age group prevalence is 5-6% in males and 2.5% in females. Dr. Bower also predicted that he sees HCV clinical presentation peaking in about 2010.

The next area that Dr. Bower covered was transmission of HCV. He stated that the following were routes of transmission:

  • Injection Drug Use
  • Clotting factors before viral inactivation (until screened for HCV)
  • Transfusion (before HCV screening)
  • Therapeutic (contaminated equipment and unsafe injection practices)
  • Occupational needle sticks
  • Perimucosal transmission
  • Perinatal 6%(not as high a risk rate as HIV which is 15-20%)
  • Sexual
  • Acute transmission
  • Injection drug use (65%) – 2 months after initiating injection drugs there is a 50% HCV infection rate and after 6 months, a 90% infection rate
  • Sexual transmission 15% - 20%
  • Others including transfusion is extremely low

Next Dr. Bower covered the incidence of HCV and HIV infection by special population
  % HCV Infection % HIV Infection
IDU 60% 31%
Men who have sex with men (MSM) Unclear 47%
Heterosexual sex 20% 10%
Transfusion before 1992 7-20% 2%
Occupational < 1% < 1%
Unknown 10% 9%

Dr. Bower stated that not all HIV positive persons are at risk for HCV. If an HIV positive person is an IDU or a hemophiliac there is an approximately an 80% risk of HCV infection. If an HIV positive man has sex with men then there is a 3-4% risk of HCV infection. He also stated that of the HCV positive people, approximately 10% are also HIV positive and of the HIV positive people approximately 25% are HCV positive. He felt that this was related to routes of transmission and the fact that HCV is more infectious.

Dr. Bower also commented that in patients that are coinfected with HIV/HCV if you look at a Metavir fibrosis grade over time, up until 4 – 5 years the progression appears to be similar to HCV. After that time the progression in the HIV/HCV coinfected patient becomes more rapid. These studies where designed prior to HAART in the protease inhibitor days. It is believed that HAART could change the outcome of disease progression. Dr. Bower concluded by stating that unlike HCV that will clinically peak in 2010, HIV/HCV will peak much earlier.

After the session, Jules Levin from NATAP, a patient advocate challenged the rate of sexual transmission of HCV being negligible with men who have sex with men. Mr. Levin stated that he believes the studies were underpowered and did not clearly define high-risk sexual behavior.

Mr. Allan Clear from the Harm Reduction Coalition commented that injection drug users are being incarcerated rather than treated and that needles are being driven off the streets of America by government. This is leading to an increased risk of infections for injection drug users. It was stated that the government’s position on injection drug use is making medical entities to help users take a back seat.

Session Three: The Natural History and Pathogenesis of HIV: A Paradigm for HCV Dr. Michael Saag, University of Alabama at Birmingham

Dr. Saag’s first comments were around the mechanism of action of all available antiretroviral therapies. He stated that such therapies only protect the uninfected cell from becoming infected and that no therapies work directly on the infected DNA cell in HIV.

In HIV there is a linear relationship between plasma viral load and HIV RNA cells regardless of the treatment. Even when a viral load is as low as 1 copy/ml there will still be about 250,000 cells in the body replicating the HIV virus. In such a case, if therapy is stopped, even though levels are considered undetectable the virus will rebound. It used to be thought that if virus was suppressed to undetectable levels for 4 years then maybe HIV could be eradicated. It is currently believed according to Dr. Saag that anti viral treatment can only suppress 99.9% of the HIV virus, which allows enough daily replication to keep HIV as a chronic disease. Based upon this determination, supportive therapy and control of HIV as a chronic disease is very important. Dr. Saag stated that early treatment maintains strong levels of CD4 T-helper cells, which in turn causes maintenance of CTL. The role of CTL is that it recognizes HIV surface antigen and will attack it. In the absence of strong CD4 T-helper cells, CTL will decline and this will cause an acute viremia, as no longer the HIV surface antigen will be attacked.

Dr. Marion Peters asked if there was any information regarding HIV transmission in intracellular hepatocytes. Dr. Saag said that he would guess that the transmission within the liver would be similar to any other lymphoid tissue. He also stated that this has been documented in the spleen. Dr. Doug Dieterich added that the effect of transmission has been documented in the liver and HIV has been found to be present in the Kupffer cells of the liver.

Part two of this report will focus on four sessions:

  • Session Four: HCV/HIV Coinfection Among Persons with Hemophilia
    Dr. James Goedert
  • Session Five: Basic Virology of HIV and HCV: Parallels and Contrasts?
    Dr. Jack Stapleton
  • Session Six: Immune Responses Against HIV and HCV: What Lessons Can We Learn From These Different Viruses?
    Dr. Margaret Koziel
  • Session Seven: Hepatitis C: Diagnosis and Evaluation
    Dr. Kenneth Sherman

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