The five immunological and inflammation gene sets (iCNV-5) again ranked topmost. ...
... t
here is a loss of genomic copies in the interferon alphas (IFNA10, IFNA14, IFNA2, IFNA21, IFNA4, IFNA5, IFNA6, IFNA8, IFNA17) and gain of copies in the “C-C” motif chemokine ligands (CCL1, CCL11, CCL13, CCL2, CCL7, CCL8) as summarized in
Table 1. Several of these chemokines have been found to be overexpressed in inflammatory diseases ... The loss of interferon alpha copies, usually implicated in the response to viral infection and another component of innate immunity, could also account for a dysregulated, secondary or compensatory response of interferons and chemokines. Several of these messengers “…are produced by neurons and glia in the adult brain, and that they can acutely influence synaptic transmission.
... The above could be suggestive of a link between in utero infections and brain development in the child. Thus, the genetic background by itself would not be enough via this view to cause a deranged developmental process which would rather only occur in the presence of relevant infections. Interferons are important in the control of viral infections via the induced expression of interferon-stimulated genes
[40]. The loss of copy number in the interferon genes suggests a possible reduced expression of such genes when stimulated. Thus, a viral infection would last longer under such a genetic background. Viral infections also lead to the expression of various chemokines in the CNS
[41]. Further, chemokines are also involved in brain development
[27],
[41]. There would therefore be a longer generation of chemokines and other cytokines that could interfere with normal brain development. Further, gain in copy number in chemokines may lead to higher levels of these chemokines and would thus exacerbate the derangement in brain development. ....