When it comes to sexual health, the virus that causes those tingling blisters and angry sores of genital herpes is often the most reviled and feared.
Most cases of genital herpes in humans are caused by the herpes simplex virus 2 (HSV-2), which affects around 12% of Australian adults.
With a reputation for causing unpredictable and unsightly outbreaks in the nether regions and the fact that it stays with you for life, it’s little wonder people are often reluctant to divulge that they have the condition. Telling prospective partners can be more excruciating than the condition itself.
Whereas HSV-2 is responsible for most cases of genital herpes, its close cousin, HSV-1, tends to stay above the belt, causing facial cold sores.
HSV-1 and HSV-2 belong to a large family of viruses that we and other animals have been evolving alongside for millennia – the herpesviruses. This nasty family of ultramicroscopic pathogen has evolved to cause brain-swelling encephalitis in cattle, respiratory disease and paralysis in horses and conjunctivitis in goats. Birds get herpes, cats get herpes. Even kangaroos get herpes.
In the late 1960s, researchers observed that HSV-1 and HSV-2 viruses clearly occupied their own distinct territories on the human body. This is still largely true, although the two viruses are increasingly squatting on each other’s turf. In 1994, less than 30% of Australian genital herpes cases were caused by the usually facial HSV-1, but by 2006, the number was over 40%.
The two viruses are somewhat unique in having evolved to occupy distinct ecological niches on the same host. In our primate relatives, and presumably our distant ancestors, a single virus infects both mouth and genitals. This comes from a lifestyle of frequent genital inspection and oral sex between males and females, and a compact body that allows for self-grooming and auto-fellatio. There was never much distance between face and privates for our forebears.
But gradually, through changes in behaviour and habit, our genitals and mouths became isolated, allowing HSV-1 and HSV-2 to become the genetically distinct viruses that they are today. Walking upright deprived us of the kind of flexibility we more often see in dogs and cats that indulge in self-grooming. And our ancestors’ proclivity for oral sex was replaced with a preference for face-to-face sex and kissing, keeping mouths with mouths and genitals with genitals.
Today, with sexual norms once again changing, our predilection for oral sex is more than likely behind the increasing rates of HSV-1 below the belt, and HSV-2 above.
As many a hapless victim will attest, the first outbreak of genital herpes is usually the worst. The virus infects the delicate skin and mucous membranes of the genitals, causing watery blisters four to seven days after exposure. Blisters can occur on the penis in men, and labia, clitoris, and vulva in women, but infections can also occur in the anus, or on the buttocks and inner thighs.
In addition to the blisters, which eventually harden and heal over a period of two to three weeks, the initial infection can cause fever, headache, muscle pain, swollen lymph nodes and fatigue.
All herpesviruses establish lifelong infections in their host, lurking out of sight of the immune system during periods of latency and bursting forth in orgies of viral reactivation and replication that cause fresh bouts of the tell-tale blisters.
The alpha subfamily of herpesviruses, of which HSV-1 and HSV-2 are members, are neurotropic viruses – they pitch camp in nerve cells during latency. After the initial infection, virus particles travel away from the sensory nerve endings at the skin surface, along the spindly nerve axon to the nucleus in the bulbous nerve body where they lay dormant. During latency, the virus is not only able to evade immune detection, but it also prevents the nerve cell from dying, ensuring that its residence will be a long one.
Re-activation is infuriatingly unpredictable – though factors such as stress and illness can provoke flare-ups. Fresh outbreaks can occur multiple times per year for some, and hardly ever for others. Fortunately, the frequency of outbreaks usually decreases over time.
While viral shedding – the release of viral particles capable of infecting a partner – is greatest during active outbreaks, it is now recognised that transmission from one person to another can occur at any time. The latency period is more like a leaky tap than a closed faucet when it comes to shedding.
Combine this with the fact that shedding can occur in areas not covered by condoms, and that researchers have so far failed to develop an effective vaccine, and it’s easy to see why herpes remains a frustratingly difficult infection to control.
Fortunately, up to 80% of people who contract HSV-2 – or HSV-1, for that matter – remain completely asymptomatic. For the remaining 20%, antiviral drugs can lessen the duration and severity of outbreaks, and although embarrassing, the virus does not cause long-term damage. We have lived with HSV-1 and HSV-2 for at least the last eight million years, and it seems likely that we will coexist for a while yet.