Source Tracking of Chicken Infectious Anemia Virus in a SPF Chicken Population, the Latest Report in China

BackgroundLive attenuated vaccines have been extensively used to prevent infectious disease in poultry flocks. However, exogenous virus contamination in attenuated vaccines had been reported several times in the past, which brought enormous threat to poultry production and diseases prevention and control. Recently, an attenuated vaccine against Newcastle Disease produced in China was detected contamination with chicken infectious anemia virus (CIAV) in a routine inspection for exogenous virus. To understand the multiple routes of transmission of CIAV, and to better formulate correct prevention and control, it is necessary to find out the possible source of this contamination.Methodslood samples of SPF chickens that generated vaccines were collected to investigate CIAV antibody titers by ELISA test. Then, 14- to 18-day-old SPF chicken embryos (n=40) were randomly selected, DNA was extracted and detected by quantitative real-time PCR and nucleic acid dot hybridization assays. To further investigate the molecular features of the CIAV isolate, the complete genome of CIAV was amplified and analyzed.ResultsThe results showed both SPF chickens and embryos for vaccine preparation were CIAV-positive. In addition, the full-length genome sequences of CIAV from vaccines and SPF chicken embryos were consisted of 2,298 nucleotides (nt) with 100% homology, named as SDSPF2020 (Genbank accession number: MW660821). It demonstrated 95.7%-99.6% homology with the complete nucleotide sequences of reference strains, and shared the closest evolution relationship with the Chinese strain HLJ15125. ConclusionThis study illustrated that vertical transmission of CIAV from SPF chickens and embryos was an important way for exogenous virus contamination in vaccine production. As such, vaccine quality monitoring and health control are significant in the poultry industry from an environmental safety point of view.

Recent developments linking retroviruses to human breast cancer: infectious agent, enemy within or both?

Evidence is accumulating that one or more beta-retrovirus is associated with human breast cancer. Retroviruses can exist as an infectious (exogenous) virus or as a part of the genetic information of cells due to germline integration (endogenous). An exogenous virus with a genome that is highly homologous to mouse mammary tumour virus is gaining acceptance as possibly being associated with human breast cancer, and recently furnished evidence is discussed in this article, as is the evidence for involvement of an endogenous human beta-retrovirus, HERV-K. Modes of interaction are also reviewed and linkages to the APOBEC3 family are suggested.

Receptor-Mediated Interference Mechanism Responsible for Resistance to Polytropic Leukemia Viruses inMus castaneus

ABSTRACT The Asian mouse Mus castaneus is resistant to infection by the polytropic mink cell focus-inducing (MCF) subgroup of murine leukemia viruses (MuLVs). Genetic crosses showed this recessive resistance to be governed by a single gene that maps at or near the gene encoding the polytropic viral receptor, Rmc1. To investigate this resistance, we mated M. castaneus with mice carrying the wild mouse Sxv variant of theRmc1 receptor that allows infection by xenotropic as well as polytropic virus. Unlike other F1 hybrids of M. castaneus, these F1 mice were resistant to both xenotropic and polytropic classes of MuLVs. Analysis of backcrossed progeny of the F1 hybrids mated to Sxv mice indicates that resistance is due to inheritance of two M. castaneus genes. Cells from individual backcross mice were also examined for cell surface antigen by fluorescence-activated cell sorter analysis with monoclonal antibodies reactive with xenotropic or MCF virus env glycoproteins. A correlation was observed between virus resistance and antigen, suggesting that virus resistance is due to expression of endogenous viral envelope genes that interfere with infection by exogenous virus. Since the inbred strain Rmc1receptor remains functional in the presence of these M. castaneus genes, and since M. castaneus contains multiple copies of xenotropic MuLV env genes, we suggest that these resistance genes control expression of xenotropicenv glycoprotein that interferes with exogenous virus in cells containing the Sxv variant of Rmc1.

Sequence comparison in the crossover region of an oncogenic avian retrovirus recombinant and its nononcogenic parent: genetic regions that control growth rate and oncogenic potential.

NTRE 7 is an avian retrovirus recombinant of the endogenous nononcogenic Rous-associated virus-0 (RAV-0) and the oncogenic, exogenous, transformation-defective (td) Prague strain of Rous sarcoma virus B (td-PrRSV-B). Oligonucleotide mapping had shown that the recombinant virus is indistinguishable from its RAV-0 parent except for the 3'-end sequences, which were derived from td-PrRSV-B. However, the virus exhibits properties which are typical of an exogenous virus: it grows to high titers in tissue culture, and it is oncogenic in vivo. To accurately define the genetic region responsible for these properties, we determined the nucleotide sequences of the recombinant and its RAV-0 parent by using molecular clones of their DNA. These were compared with sequences already available for PrRSV-C, a virus closely related to the exogenous parent td-PrRSV-B. The results suggested that the crossover event which generated NTRE 7 took place in a region -501 to -401 nucleotides from the 3' end of the td-PrRSV parental genome and that sequences to the right of the recombination region were responsible for its growth properties and oncogenic potential. These sequences included a 148-base-pair exogenous-virus-specific region that was absent from the RAV-0 genome and the U3 region of the long terminal repeat. Since the exogenous-virus-specific sequences are expected to be missing from transformation-defective mutants of the Schmidt-Ruppin strain of RSV, which, like other exogenous viruses, grow to high titers in tissue culture and are oncogenic in vivo, we concluded that the growth properties and oncogenic potential of the exogenous viruses are determined by sequences in the U3 region of the long terminal repeat. However, we propose that the exogenous-virus-specific region may play a role in determining the oncogenic spectrum of a given oncogenic virus.