Further reading
Palacios, Druce, Du, Tran, Birch, Briese, Conlan, Quan, Hui, Marshall, Simons, Egholm, Paddock, Shieh, Goldsmith, Zaki, Catton, Lipkin (2008). "A New Arenavirus in a Cluster of Fatal Transplant-Associated Diseases". The New England Journal of Medicine. 358 (10): 991–998. doi:10.1056/NEJMoa073785. PMID 18256387. {{cite journal}}:  CS1 maint: multiple names: authors list (link)

External links
Virus Pathogen Database and Analysis Resource (ViPR): Arenaviridae
When the mutation is present, there is no signal for B cells to undergo class switching, so there is an excess of IgM and little to no other immunoglobulin types produced. Type 4
Immunodeficiency with hyper IgM type 4 is poorly characterized. All that is known is that there is an excess of IgM in the blood, with normal levels of the other immunoglobulins. The exact cause is yet to be determined. Type 5
Immunodeficiency with hyper IgM type 5 is caused by a mutation in the Uracil-DNA glycosylase (UNG) gene, which, like AICDA, is located on chromosome 12. This codes for Uracil DNA Glycosylase, which is responsible for excising previous uracil bases that are due to cytosine deamination, or previous uracil misincorporation from double-stranded previous DNA substrates. This enzyme is also responsible for helping with gene conversion during somatic recombination in B cells. The mutation in the gene causes an enzyme that does not function properly, thus gene conversion does not proceed and class switching cannot occur. See also
Monoclonal gammopathy of undetermined significance

References


== External links ==