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Mannan‐binding lectin modulates the response to HSV‐2 infection

Viruses have developed numerous strategies to escape recognition by the immune system. However, some viruses such as herpes simplex virus‐2 (HSV‐2) are recognized by initiators of the complement system, e.g. mannan‐binding lectin (MBL). To study the effects of MBL deficiency during viral infection we have chosen a model of generalized HSV‐2 infection. We infected MBL‐A and MBL‐C double knock‐out mice (DKO) with HSV‐2 via the intraperitoneal (i.p.) route. DKO mice cleared HSV‐2 from the liver less efficiently than the comparable wild‐type animals. The impairment to effectively neutralize HSV‐2 correlated with compromised liver function as measured by increased plasma levels of alanine‐amino transferase. No differences in the viral burden were found in other organs such as spleen or brain. Thus, MBL‐mediated protection was limited to the effects of preservation of liver homeostasis. Reconstitution with recombinant human MBL before and during the HSV‐2 infection dramatically lowered the viral titres in the liver. Taken together, the data show that MBL modulates the response to HSV‐2 in mice by affecting neutralization of the virus. To analyse if MBL plays a role in establishment and progression of human HSV‐2 infection we analysed MBL levels in the serum samples from asymptomatic (virus‐exposed people who have never displayed symptoms of HSV‐2 infection) and symptomatic HSV‐2 patients (people with recurrent HSV‐2 infections). We found that the frequency of the MBL deficiency (<100 ng/ml) was higher in the symptomatic group and significantly different from that in the asymptomatic group (P = 0·0369). This suggests that lack of MBL‐mediated complement activation increases susceptibility to viral infection.