![]() illustration: ron meerbeek |
A scary new monster is on the loose among HIV positive gay men, shattering assumptions that HIV was the baddest bug on the block. It’s called sexually-transmitted hepatitis C, and Dr Mark Nelson of London’s Chelsea and Westminster Hospital tells Gus Cairns why we should beware of it
Well, sexual transmission of hep C is something that’s been very ignored in the past. People just assumed it was a disease of intravenous drug users. There was no way of proving it did happen, so people assumed it didn’t.
Yet we’ve always known that those who live with people with hep C are more likely to get it themselves, even if they’ve never injected drugs. We didn’t know how it happened. Sharing toothbrushes? Coke straws? Or sex?
But suddenly something new has happened in the last two years. We have seen acute - that is, recently contracted - cases of hep C among the gay men coming to the clinic. And similar outbreaks have been reported in Germany and Australia. We know they’re new infections because we didn’t start suddenly testing more people for hep C antibodies; we’ve always done that to some extent.
What has happened? A change in the virus? No, because people are not catching a single viral strain, it’s the usual mixture of genotypes. (Note: hep C comes in about six varieties, of which genotypes one and four are the hardest to treat).
We’re doing a study with the Royal Free Hospital to analyse the genetic makeup of viruses more precisely. The RFH has already found that some infections are of almost identical virus, which makes it look like they originated in a single person or group of people.
So we think that the likeliest explanation is a change in sexual practices among HIV positive gay men.
I’d be careful about attributing it all to ‘barebacking’. The answer is we simply don’t know exactly how it’s being transmitted at present, and need to do studies to find out.
In the people I’ve seen, there is a high incidence of fisting, but that’s anecdotal, we don’t know how many people are into fisting who don’t have hep C.
I don’t want to worry PN’s readers or say they should be taking additional precautions; the same safer sex rules should protect you, as far as we know. But we are starting to see it in out-of-London centres like Brighton, which is worrying. The question is why is it suddenly being sexually transmitted now?
In the population at large, we simply don’t know. (Ed: public health experts have estimated that 90 per cent of hep C in the UK remains undiagnosed, compared with 33 per cent of HIV, and 25 per cent of HIV among gay men).
All I can say is that we’ve seen 56 cases of acute hep C infection among clinic attendees, and that’s more than one per cent of the patient group.
It’s being seen as a disease of HIV positive gay men. But a lot of it is being picked up because people on HIV medications get liver function tests, and we see these sudden liver flare-ups that aren’t drug related. But if you go to a GUM clinic you won’t get a liver function test, so cases among the HIV negative population may be missed.
However it certainly looks as if the risk of transmission of hep C is greater if you already have HIV. And HIV positive people with hep C tend to have higher hep C viral loads in semen and are therefore more infectious, especially if they also have low CD4s.
But there are increasing numbers of heterosexuals with HIV and they’re not getting hep C, so it’s not just about viral loads. It must be behaviour.
Well, about 25 per cent of people with hep C clear their virus spontaneously, and in our acutely infected patients it’s more like 45 per cent.
For those who don’t, in acute infection, if it’s caught early, the cure rate in HIV negative people who are given the gold-standard therapy of pegylated interferon and ribavirin is nearly 100 per cent. But in our patients with HIV, it’s only been 56 per cent.
In chronically infected patients with HIV and hep C, the cure rate in studies is only 45 per cent, and is lower with genotypes one and four; but many of those studies didn’t use ribavirin.
We have had two deaths due to hepatitis C in our clinic in the last month. But both of those were chronically-infected patients who had continued to drink alcohol. At present, even our chronic patients are doing reasonably well.
In many cases, the advice is ‘wait and see’. We are waiting for the results of big studies like APRICOT (results due in February) which look at treatment in co-infected people.
We take a liver biopsy and if the liver is not in difficulties and the patient is not keen on getting treatment right away, we say wait. Or we say, give it a go, and if you feel awful, stop it. They have been recently infected so they have time, though the cure rate goes down over time.
On the other hand, hep C itself can make you feel pretty unwell. Even without liver damage, you get the usual ‘viral’ symptoms like night sweats, and there can be kidney and skin complications.
Because of this, when people start treatment, they often say, “I didn’t realise how unwell I felt till I started treatment.” Then when it’s over they say, “I didn’t realise how unwell I felt till it stopped!”
We’ve only had one patient who had to stop treatment due to drug toxicity, and that’s out of 24 on treatment. Pegylated interferon causes relatively mild depression and flu symptoms, we find, compared with old-style interferon. One should treat side effects proactively, starting antidepressants before the treatment.
The hep C treatment can interfere with your HIV treatment, too. Depression can cause poor adherence. And ribavirin interferes with some drugs, like ddI, so you might have to change your HIV regime.
No alcohol, that’s the biggest contributing factor. People need to have a life, so we say “drink as little alcohol as possible, and preferably none.” The same with recreational drugs. Ecstasy is processed by the liver; cocaine not so, but that has other health hazards! And eat a sensible low-fat diet so the liver doesn’t have to try to process lots of fat.
You should have a hep C antibody test. But remember, people with low CD4 counts sometimes don’t make hep C antibodies, so if people are hep C antibody negative but have abnormal liver function tests and/or have possibly been exposed to hep C, they should have a hep C viral load test. Some London clinics perform hep C antibody tests once a year on patients, but many others don’t test everyone, so you should ask if you’ve been tested - not ever, but recently. This is a new infection so an old negative test means nothing. People need to get used to asking for liver function tests as routinely as they get their cholesterol checked out.
It’s a different kettle of fish. It’s very common: about 50-70 per cent of HIV clinic patients will have had it at some point, but 90 per cent of patients clear it spontaneously. It looks like hep B never completely disappears from the body and we do occasionally see reactivation in people with very low CD4 counts, when it’s essentially an Aids-related opportunistic infection.
Well, hep C protease inhibitors and other drugs are coming along in the next few years. But they may not cross into the brain and hep C may reproduce there, so we may continue to use interferon.
We need to do more studies to know how it’s being transmitted and whether it’s the hep C that really is causing the liver problems we see in some people.
My advice to people is that they shouldn’t be scared, but they need to think about their sexual risk behaviour. And they need to get tested!