Disease relevance of Emv16

• During the derivation of an SWR/J strain congenic for Emv-16 and Emv-17, we found that many of the progeny derived from female virus carriers acquired new germline ecotropic proviruses [1].
• Exogenous infection of SWR/J mice with either Emv-16 or Emv-17 leads to viremia in the host animals, and in both cases, progeny of viremic females acquire new proviral insertions [2].
• The endogenous ecotropic murine retroviruses Emv-16 and Emv-17 are both capable of producing new proviral insertions in the mouse genome [2].

High impact information on Emv16

• Two of these proviruses, Emv-16 and Emv-17, are tightly linked and segregate with the high viremia phenotype in backcrossed mice [1].
• The frequency of provirus acquisition in Srev lines that expressed the infectious ecotropic virus was similar to that in SWR.RF mice carrying Emv-16 and Emv-17, suggesting that the chromosomal integration site of the parental locus is not an important determinant for high-frequency provirus acquisition [3].
• New germ line proviral insertions are acquired at a high frequency by the progeny of SWR/J-RF/J hybrid female mice that carry the endogenous ecotropic murine leukemia proviruses Emv-16 and Emv-17 [2].

Biological context of Emv16

• A comparison of the flanking cellular DNA suggests that the Emv-16 and Emv-17 loci did not arise by simple duplication of a viral insertion site within the RF/J genome but most likely are independent integration events [2].

References