Virus dou­bles risk of hav­ing autis­tic child: study

Preg­nant wo­man’s im­mune re­sponse to gen­i­tal her­pes can af­fect fe­tus

The Hamilton Spectator - - A&E - IS­ABEL TEOTONIO

Women who be­come in­fected with gen­i­tal her­pes dur­ing early preg­nancy, or ex­pe­ri­ence a flare-up of the sex­u­ally trans­mit­ted dis­ease, have twice the risk of giv­ing birth to a child later di­ag­nosed with autism, ac­cord­ing to a new longitudinal study pub­lished Wed­nes­day.

The study, led by the Cen­ter for In­fec­tion and Im­mu­nity at Columbia Univer­sity, is the first to make the link be­tween a preg­nant wo­man’s im­mune re­sponse to a virus and the risk of her off­spring de­vel­op­ing autism spec­trum dis­or­der (ASD).

“We be­lieve the mother’s i mmune re­sponse to HSV-2 (gen­i­tal her­pes) could be dis­rupt­ing fe­tal cen­tral ner­vous sys­tem de­vel­op­ment, rais­ing risk for autism,” says lead au­thor Mi­lada Mahic, a post­doc­toral re­search sci­en­tist with the cen­tre and also the Nor­we­gian In­sti­tute of Public Health.

Pub­lished in mSphere, a jour­nal of the Amer­i­can So­ci­ety for Mi­cro­bi­ol­ogy, the study sheds light on ASD, a group of com­plex neu­ro­log­i­cal dis­or­ders char­ac­ter­ized by dif­fi­cul­ties with com­mu­ni­ca­tion, so­cial chal­lenges and a ten­dency to re­peat spe­cific be­hav­iours. About one in 68 di­ag­nosed chil­dren is on the autism spec­trum, ac­cord­ing to Autism Speaks Canada.

“The cause, or causes, of most cases of autism are un­known,” says se­nior au­thor Dr. Ian Lip­kin, who’s also direc­tor of the cen­tre. “But ev­i­dence sug­gests a role for both ge­netic and en­vi­ron­men­tal fac­tors. Our work sug­gests that in­flam­ma­tion and im­mune ac­ti­va­tion may con­trib­ute to risk. Her­pes sim­plex virus-2 could be one of any num­ber of in­fec­tious agents in­volved.”

In Canada, about 16 per cent of fe­males aged 14 to 59 have gen­i­tal her­pes, ac­cord­ing to Statis­tics Canada. For some, the life­long in­fec­tion can cause painful sores on the gen­i­tal area, while oth­ers have no symp­toms or vis­i­ble sores. Af­ter sores from the first at­tack heal, the virus goes into a dor­mant stage, but re­cur­rent out­breaks can oc­cur, ac­cord­ing to Health Canada.

The study’s au­thors looked at blood sam­ples from 412 moth­ers of chil­dren di­ag­nosed with ASD and 463 moth­ers of chil­dren with­out ASD who are en­rolled in the Autism Birth Co­hort (ABC) Study con­ducted by the Nor­we­gian In­sti­tute of Public Health. (The study is part of the larger Nor­we­gian Mother and Child Co­hort Study, in which some 90,000 preg­nant women were re­cruited be­tween 1998 and 2008 to help with the study of dis­ease.)

They stud­ied sam­ples taken around 18 weeks of preg­nancy and at birth, look­ing for a link be­tween ma­ter­nal in­fec­tion and the risk for ASD. They fo­cused on a group of in- fec­tious agents that can cause mis­car­riage and birth de­fects, known col­lec­tively as TORCH: Tox­o­plasma gondii, Rubella, Cy­tomegalovirus and Her­pes Sim­plex viruses type 1 (HSV-1 or oral her­pes) and type 2 (HSV-2 or gen­i­tal her­pes).

They looked at the lev­els of an­ti­bod­ies to each of the TORCH pathogens and found high lev­els of HSV-2 an­ti­bod­ies cor­re­lated with in­creased risk for ASD in boys. (There were too few fe­males with ASD for re­searchers to con­clude if the ef­fect is sex-spe­cific.) This link was only ev­i­dent in the blood sam­ples taken dur­ing mid-preg­nancy. Be­cause it takes weeks for the body to make large amounts of an­ti­bod­ies, in­fec­tion — or re­ac­ti­va­tion of in­fec­tion — oc­curred dur­ing early preg­nancy, when the fe­tal ner­vous sys­tem is un­der­go­ing rapid de­vel­op­ment.

The study’s au­thors sug­gest that pla­cen­tal in­flam­ma­tion, ex­po­sure of the fe­tus to in­flam­ma­tory mol­e­cules pro­duced by the pla­centa, or the trans­fer of ma­ter­nally pro­duced an­ti­bod­ies across the pla­centa, can cause fe­tal brain in­flam­ma­tion and in­crease the risk for ASD.

“There’s no ev­i­dence that this virus is ac­tu­ally go­ing in to in­fect the fe­tus,” says Lip­kin, adding such trans­mis­sions are rare and typ­i­cally re­sult in fe­tal death in utero.

“The im­por­tant fac­tor here is not the virus it­self, but the im­mune re­sponse to the virus that is caus­ing the dam­age.

“What we’re re­ally do­ing is propos­ing a model that we think is go­ing to be generic for un­der­stand­ing how these things might oc­cur. And it likely has im­pli­ca­tions for a wide range of other sorts of sys­temic dis­or­ders.”

DREAMSTIME

The longitudinal study is the first to make the link be­tween a preg­nant wo­man’s im­mune re­sponse to a virus and the risk of her off­spring de­vel­op­ing the dis­or­der.

HANDOUT

Dr. Ian Lip­kin, above, says it’s not the virus it­self, but the mother’s im­mune re­sponse to it that raises the risk for autism in the fe­tus.

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