International Meeting for Autism Research: Association of Autism with Polyomavirus Infection in Postmortem Brains

Association of Autism with Polyomavirus Infection in Postmortem Brains

Saturday, May 22, 2010: 10:00 AM
Grand Ballroom AB Level 5 (Philadelphia Marriott Downtown)
9:45 AM
C. Lintas , Univ. Campus Bio-Medico, Rome, Italy
L. Altieri , Univ. Campus Bio-Medico, Rome, Italy
F. Lombardi , Univ. Campus Bio-Medico, Rome, Italy
R. Sacco , Univ. Campus Bio-Medico, Rome, Italy
A. M. Persico , Univ. Campus Bio-Medico, Rome, Italy
Background: Autism is a highly heritable behavioural disorder. Yet, very few cases can be solely explained on the basis of de novo genetic mutations or cytogenetic abnormalities. Environmental factors interacting with the genetic background of each individual can contribute to explain familiality in the presence of genomic instability and low rates of disease-specific genetic mutations.
Objectives: To assess the presence of neurotropic viruses in post-mortem brains of autistic patients and matched controls.
Methods: We assessed by nested-PCR and DNA sequence analysis the presence of CMV, EBV, HSV1, HSV2, HHV6, BKV, JCV, and SV40 in genomic DNA extracted from post-mortem temporocortical tissue (Brodmann Areas 41/42) belonging to 15 autistic patients and 13 controls.
Results: BKV, JCV, and SV40 combined are significantly more frequent among autistic patients compared to controls (67% vs 23%, respectively; P<0.05). No difference is recorded for all other viruses, which are found in relatively few individuals (N≤3). Also poly-viral infections tend to occur more frequently in the brains of autistic patients compared to controls (40% vs 7.7%, respectively; P=0.08).

Conclusions: Polyomaviruses are over-represented in our sample of autistic post-mortem brains compared to controls; autistic brains also display higher frequencies of positivity to more than one virus. Hence polyomaviruses represent attractive candidates for follow-up studies exploring gene x environment interactions as possible contributors to autism pathogenesis.

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