ABSTRACT
To understand the genetic diversity of porcine deltacoronavirus(PDCo V) in Guangxi Province, clinical diarrhea samples were collected from suspected piglets in Guangxi Province from2017 to 2019, detected by RT-PCR for PDCoV, and the positive samples were used for amplification and sequence of S, M, N genes. Finally, 16 S, M and N gene sequences of PDCoV were obtained. Homology analysis showed that the S, M, N gene nucleotide identity among Guangxi strains were 95.8% -99.9%, 95.9%-100% and 97.9%-99.9%, respectively. The nucleotide identity of S, M and N genes among Guangxi strains and other reference strains were 95.1%-100%, 95.0%-100%and 96.3%-99.9%, respectively. Sequence alignment showed that S1 protein existed amino acid mutations and insertions, and there were some variations among different epidemic strains. Phylogenetic trees based on S, M and N genes obtained similar topological diagram and all strains could be divided into Group I, Group II and GroupIII, of which Group I came from USA, Japan and Korea, Group II came from China, and Group III came from China, Vietnam, Laos and Thailand. Most strains from Guangxi Province distributed in Group II, individual strain distributed in Group III and some strains formed a single small branch. The evolutionary rates of S, M and N genes of Guangxi strains and other reference strains were 2.57 x 10-4, 2.07 x 10-4, 1.70 x 10-4 substitutions/site/year, respectively, showing that the evolutionary rate of S gene was the fastest. The results indicated that the S, M, N genes of PDCo V strains from Guangxi Province had some variations and existed genetic diversity.
ABSTRACT
The wide spread of viral infections and the ease of overcoming the species-specific barriers require the identification of critical stages in the virus interaction with multicellular organisms of mammals and the analysis of key molecular genetic systems involved. To date, a large amount of data has already been accumulated on the diversity and complexity of such systems, as well as the involvement in them the wide range of metabolic pathways. In this regard, attempts to identify some common elements that are implemented in different infectious processes are of particular relevance. This paper is such attempt made on the example of the analysis of the main events of cattle infection by bovine leukemia virus (BLV). Systems involved in the entry of BLV genetic material into the cytoplasm of host cells, the suppression of innate and adaptive immunity, as well as interactions between the genomes of the BLV provirus and the host genome are the identified critical stages. The direct participants in the reception of viral proteins are parts of some host tansmembrane systems (G.Yu. Kosovsky et al., 2017;V.I. Glazko et al., 2018;L. Bai et al., 2019;H. Sato et al., 2020). During virus reproduction in host cells, host enzymes modify virus envelope proteins by (A. De Brogniez et al., 2016;W. Assi et al., 2020). Importantly, modifications of SARS-CoV-2 spike proteins, as well as BLV envelope proteins, have a significant impact on their pathogenicity (M. Hoffmann et al., 2020). Pathogenicity and depressing effect of both BLV and SARS-CoV-2 on innate and adaptive immunity is realized in part through the activation of T regulatory cells and an increase in the expression of the growth transforming factor TGF-b (L.Y. Chang et al., 2015;G.Yu. Kosovsky et al., 2017;W. Chen et al., 2020). Intracellular mechanisms of protection against retrotranspositions, recombinations between viruses and host retrotransposons, the formation of new elements of host regulatory networks such as microRNAs, and the integration of proviral DNA into the host genome are closely related and controlled by interfering RNA (RNAi) systems with the key gene dicer1 (P.V. Maillard et al., 2019;E.Z. Poirier et al., 2021;G.Y. Kosovsky et al., 2020). These systems can provide a certain left-pointing-double-angle resistance right-pointing-double-angle of the host genome both to the integration of exogenous genetic material and to transpositions of own mobile genetic elements. Apparently, it is the polygenicity of the control of these critical stages of viral infection that leads to difficulties in predicting their development and developing methods for their prevention.