Endogenous Retrovirus-like Sequences Research Articles

Human endogenous proviruses.

The present concern about human immunodeficiency viruses and human T-cell leukemia viruses has generated renewed interest in human endogenous retroviruses, or HERVs. The DNA of humans contains perhaps thousands of endogenous retro-viruses (ERVs) or retrovirus-like sequences which are detectable by their homology to retroviruses of other vertebrates. A number of these ERVs have been isolated, partially or completely sequenced, and their messenger (m)RNA products characterized. The HERVs studied thus far are all defective proviruses, and it is unlikely that there are many infectious ERVs in human DNA. For example, transfection in indicator cells of DNAs isolated from nonviremic human sarcomas and leukemias did not result in retroviral replication in the recepient cells (Nicolson et al. 1978). HERVs, then, are chromosomal elements that are inherited as Mendelian traits and, for the most part, encode defective retroviruses. In contrast to the case in humans, infectious ERVs have been demonstrated in the genome of such vertebrates as mice (see Konzak 1985), chickens (Weiss et al. 1971), and baboons (Nicolson et al. 1978; Cohen et al. 1981).KeywordsFollicular FluidMouse Mammary Tumor VirusMurine Mammary Tumor VirusDefective ProvirusSimian Sarcoma VirusThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Chromosomal distribution of the RTVL-H family of human endogenous retrovirus-like sequences

We have analyzed the chromosomal distribution of a large family of human endogenous retrovirus-like sequences termed RTVL-H. In situ hybridizations suggest that these sequences are found on all human chromosomes. These results also indicate that clusters or concentrations of RTVL-H elements may exist on chromosomes 1p and 7q. Southern blotting experiments using somatic cell hybrids containing either the human chromosome 3 or the X chromosome confirm the presence of multiple dispersed RTVL-H sequences on these two chromosomes. These experiments also demonstrate that distinct RTVL-H banding patterns can be detected for each chromosome. Thus, RTVL-H probes may be useful in genome mapping studies.

Isolation of three kinds of human endogenous retrovirus-like sequences using tRNA(Pro) as a probe.

Three kinds of human endogenous retrovirus-like sequences (HuERS-P1, 2 and 3) were isolated from a HeLa cell genomic library using the 3'-half fragment of proline tRNA as a hybridization probe. These elements contained putative primer binding sites complementary to the 3'-terminus of proline tRNA and long terminal repeats (LTRs) characteristic of retrovirus provirus. The LTR sequence of HuERS-P1 consisted of about 690 nucleotides and contained a CAT box, a TATA box and a polyadenylation signal. A complete unit of an Alu family sequence was inserted into the 5'-LTR of one of the clones. HuERS-P2 also contained a TATA box and a polyadenylation signal in its LTR (about 840 nucleotides long), but the LTR sequence of this element was quite different from that of HuERS-P1. Although clone HuERS-P3 contained only the 5'-LTR region, this LTR sequence contained a CAT box, a TATA box and a poly-adenylation signal and was quite similar to the LTR sequence of the recently isolated human retrovirus-related sequence HuRRS-P (Kröger, B. and Horak, I. (1987) J. Virol., 61, 2071-2075). Human and simian DNAs contain 10 to 40 copies of these elements, but mouse DNA does not contain these elements.

Retroviruses as Chromosomal Genes in The Mouse

Publisher Summary The mouse retroviruses are RNA-containing viruses that replicate through a DNA intermediate. This chapter describes the four major classes of endogenous mouse retroviruses—namely, the type C mouse leukemia viruses (MuLVs), the type B mouse mammary tumor viruses (MMTVs), the intracisternal A particles (IAPs), and the virus-like endogenous sequences (VL30s). It also describes the arrangement and stability of these sequences in the mouse germline, the experimental evidence linking specific germline integrations with various polymorphic chromosomal loci, and the association of specific somatically acquired proviruses with tumor induction and progression. The mouse retroviruses are essentially classified into four groups based on differences in virion morphology— MuLVs, MMTVs, IAPs, and VL30s. The virions have type A, B, or C structure as revealed by electron microscopy. MuLVs and MMTVs are replication-competent viruses with type C and type B structures, respectively. IAPs resemble immature type B virions, but are noninfectious and are found only intracellularly. VL30s are endogenous retrovirus-like sequences that are not known to produce any virion structural components, but can be efficiently packaged and transmitted as pseudotypes of type C viruses.

Molecular cloning of retrovirus-like genes present in multiple copies in the Syrian hamster genome.

Endogenous retrovirus-like sequences homologous to intracisternal type-A particle (IAP) genes, which are present in the inbred mouse (Mus musculus) genome, were cloned from a Syrian hamster gene library. A typical hamster IAP gene was 7 kb long and segments homologous to long terminal repeat (IAP) sequences present in Mus musculus IAP genes were located at both ends of the gene. Contrary to the pattern found in the Mus musculus IAP genes, the organization of the cloned hamster IAP genes was not markedly polymorphic and deletion was not observed among these cloned genes. A sequence about 0.8 kb long and located close to the 3' end of the hamster IAP gene was well conserved in both IAP gene families, although they showed less overall homology with one another. The reiteration frequency of the hamster IAP genes was calculated to be 950 copies per haploid genome. Since such IAP genes with the above properties were not found in the genome of the Chinese hamster, whose progenitors diverged from those of the Syrian hamster about 7.5 Myr ago, the integration of a huge number of Syrian hamster IAP genes must have occurred subsequent to such divergence.