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Jens Christian Jensenius

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

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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 (
Original languageEnglish
JournalClinical and Experimental Immunology
Volume138
Issue2
Pages (from-to)304-11
Number of pages8
ISSN0009-9104
DOIs
Publication statusPublished - 2004

    Research areas

  • Adult, Aged, Alanine Transaminase, Animals, Brain, Female, Herpes Genitalis, Herpes Simplex, Herpesvirus 2, Human, Homeostasis, Humans, Liver, Male, Mannose-Binding Lectin, Mice, Mice, Knockout, Middle Aged, Recombinant Proteins, Recurrence, Spleen, Viral Load, Viral Proteins

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