cIn China, a majority of the highly pathogenic porcine reproductive and respiratory syndrome (HP-PRRSV) strains were seeded by the 2006 outbreak. However, the most recently emerged (2013-2014) HP-PRRSV strain has a very different genetic background. It is a NADC30-like PRRSV strain recently introduced from North America that has undergone genetic exchange with the classic HP-PRRSV strains in China. Subsequent isolation and characterization of this variant suggest high pathogenicity, so it merits special attention in control and vaccine strategies. P orcine reproductive and respiratory syndrome (PRRS) is characterized by respiratory distress in nursery swine and reproductive failure in sows and has resulted in huge economic losses to the global swine industry since its first recognition in the United States in 1987 (1). In China, highly pathogenic PRRSV (HP-PRRSV) has been circulating and predominating in the field since the initial outbreak in 2006 and has resulted in the loss of more than one million pigs (2-5). Retrospective studies of that outbreak have shown that the highly pathogenic variant emerged from less pathogenic PRRSV strains in China (6), which were initially introduced from North America in the 1990s. CH-1a was the earliest representative of this group (7). Following the outbreak, more-stringent biosecurity controls and a targeted immunization campaign were undertaken to limit HP-PRRS in China.However, despite these measures, HP-PRRSV has experienced recurrent population expansions since the initial outbreak. One such reemergence was associated with genetic exchange between two HP-PRRSV viruses circulating in the field (8). Another recent outbreak (2013)(2014) is probably in the early stage of emergence. It has occurred in several provinces of China and is characterized by high fever, cough, anorexia, red discoloration of the body, and blue ears. Diseased pigs also have multiple visceral lesions. Their lungs display consolidation, and their lymph nodes are enlarged and hemorrhagic. The rates of morbidity and mortality due to this new HP-PRRSV are very high. An affected farm in Jilin Province had a morbidity rate of 100% and a mortality rate of 76.6% (230/ 300).We obtained the representative open reading frame 5 (ORF5) sequences from two farms that experienced the disease, i.e., JL580 and HLJ58 from Jilin Province and Heilongjiang Province, respectively. Phylogenetic analyses using the PhyML version 3.0 software (9) suggested that these viruses are distantly related to the classic HP-PRRSV strains in China, which belong to lineage 8 (Fig. 1A). Instead, they nested deeply within diverse lineage 1, which originated in Canada and is now prevalent in both the United States and Canada (10). Interestingly, the virus is also closely related to a group represented by NADC30, a moderately virulent strain isolated in 2008 in the United States (11). Furthermore, the phylogenetic topology of the diversity surrounding this new HP-PRRSV suggests, with high resolution, a transmission chain from Canada to the Unit...

MyD88, a key adaptor molecule required for many innate immunity receptor-activated signaling pathways, was evaluated in a Chlamydia muridarum urogenital tract infection model. Compared with wild-type mice, MyD88 knockout (KO) mice failed to produce significant levels of inflammatory cytokines in the genital tract during the first week of chlamydial infection. MyD88 KO mice developed a Th2-dominant whereas wild-type mice developed a Th1/Th17-dominant immune response after chlamydial infection. Despite the insufficient production of early inflammatory cytokines and lack of Th1/Th17-dominant adaptive immunity, MyD88 KO mice appeared to be as resistant to chlamydial intravaginal infection as wild-type mice based on the number of live organisms recovered from vaginal samples. However, significantly high numbers of chlamydial organisms were detected in the upper genital tract tissues of MyD88 KO mice. Consequently, MyD88 KO mice developed more severe pathology in the upper genital tract. These results together have demonstrated that MyD88-dependent signaling pathway is not only required for inflammatory cytokine production in the early phase of host response to chlamydial infection but also plays a critical role in the development of Th1/Th17 adaptive immunity, both of which may be essential for limiting ascending infection and reducing pathology of the upper genital tract by chlamydial organisms.

Recently pseudorabies outbreaks have occurred in many vaccinated farms in China. To identify genetic characteristics of pseudorabies virus (PRV) strains, we obtained the genomic sequences of PRV strains HeN1 and JS, which were compared to 4 PRV genomes and 729 partial gene sequences. PRV strains isolated in China showed marked sequence divergence compared to European and American strains. Phylogenetic analysis revealed that for the first time PRV can be divided into 2 distinct clusters, with Chinese strains being genotype II and PRVs isolated from other countries being genotype I. Restriction fragment length polymorphism analysis confirmed differences between HeN1 and Bartha strains, as did the presence of unique insertion/deletion polymorphisms and microsatellites. This divergence between the two genotypes may have been generated from long-term, independent evolution, which could also explain the low efficacy of the Bartha vaccine in protecting pigs infected with genotype II PRV.