Harms of HSV-2 may include association of latent infection with autism as well as transfer of active infection to the neonate

Mahic & Lipkin (M&L) draw attention to a wholly new health concern in relation to Herpes Simplex Virus 2.

The condition is highly contagious, and the symptoms may be very unpleasant especially during the ‘primary outbreak’, the virus is not, in itself, a major public health concern.  Indeed, up until the 1980s, it was rarely mentioned in this journal – perhaps because it was less common before the 1970s, or maybe because the condition was insufficiently severe to warrant much discussion.

HSV-2 owes its status as a serious health problem to two issues that are independent of its impact on the everyday sufferers.  The first concerns the potentially devastating consequences of transmission of HSV-2 to the neonate (generally in the course of birth rather than in utero) (Preventing neonatal herpes (STIs)).  These are so severe as to have led to a considerable debate on the cost-effectiveness of screening in various parts of the world (Mindel & Cunningham (STIs) (Australia);  Barnabas & Garnett (STIs) (US); Sudfeld & Mensch (STIs) (Malawi)).  The second concerns the links between HSV infection and HIV transmission.  This is an issue discussed primary in the sub-Saharan African context, where HSV is particularly prevalent and its treatment could potentially impact the HIV epidemic (White and Glynn (STIs); Lurie & Matthews (STI)) – though also in the Indian context (Foss & Watts (STI)).

To these two serious concerns Mahic & Lipkin, in a paper recently appearing in the microbiology journal mSphere, have added a third of as yet uncertain importance – the possibility of an association with male autism.  Basing their investigation on data from the Norwegian Autism Birth Cohort (comprising mothers, fathers and infants recruited over the period 1999-2008), the researchers compared maternal immunoglobulin (IgG) antibodies to HSV-2 (amongst other viruses), which had been measured in 442 mothers of male offspring with ASD mid-term, against a frequency-matched control of 464 mothers of ASD unaffected offspring.  An increase in HSV-2 IgG levels from 240 to 640 arbitrary units/ml was found to be associated with a doubling (RR=2.07) in the odds of ASD.  This was not replicated in the case of antibodies to other viruses that were tested for.

The authors suggest that it is the ‘impact of immune activation and inflammation on a vulnerable developing nervous system’ which is likely to be the mechanism here rather than ‘the specific pathogen per se’ – maybe the transfer of maternally produced antibodies and cytokines across the placenta, or the exposure of the fetus to inflammatory molecules produced by the placenta and deciduas in relation to viral shedding.

The question posed by this outcome – should it be confirmed by subsequent research – is whether this third potential harm, when added to the well-established harm of neo-natal infection, might contribute to tipping the balance in favour serological monitoring and suppressive therapy during pregnancy – at least in certain contexts (cf. Barnabas & Garnett (STIs) (US)).


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