Both mouse and human chemokine receptor CXC motif 5 (CXCR5) genes exhibit one single intron interrupting the coding sequence. The mouse intron is 12053 nucleotides (nt) long; the human intron is 9603 nt long. Sections of the mouse intron significantly align plus/plus with sections of the human intron; the aligned segments are in the same order in mouse as in man and overall cover 13% of the mouse sequence and 17% of the human sequence. The human CXCR5 intron harbors sequences derived from retroviruses (human endogenous retroviruses). The mouse intron comprises very similar sequences. About 70% of the mouse intron sequence is ‘specific’ to this gene, while sequences in the rest of the intron are shared with many other genes located on different chromosomes. In the human the coverage by specific sequences is about 87%. Thus, the contribution of transposable elements is significantly higher in mouse (30%) than in man (13%). Intra-intronic plus/minus alignments exist in mouse (10 couples) and man (two couples): these may form stem and loop structures determining the secondary structure of the corresponding premRNAs.

Some Herpes-, Pox- and Irido-virus genes (and the controversial Stealth virus gene) share significant nucleotide sequences with vertebrate chemokine receptors (CKR) genes. In some instances the viral reading frame is the same as in the CKRs, giving rise to similar protein products. In other cases the reading frame is different and the viral protein product is not CKR-like. In yet other instances the segmental alignments between CKR genes and viral genes are more limited. In this article we discuss in detail only the more highly significant alignments. We propose the hypothesis that both CKR and CKR-like viral genes originated from a common ancestral gene. This older ancestor may have differentiated into two sequences, one giving rise to the group of extant CKR genes with relatively low levels of similarity with viruses, and the other to the other extant CKRs and the CKR-like viral products. The two extant proteins of the CKR and viral groups which share the maximum amino acid identities are the human CCR3 and the E1 of the Equid herpes virus 2, with a continuous alignment coverage of 73% of the viral molecule. It is thus proposed that the ancestral sequence giving rise to both CKRs and CKR-like viral products may have been similar to the extant human CCR3 and E1 Equid herpes virus 2.