Cells infected with SFTSV also released exosomes containing virions, and when the exosomes were taken up by uninfected cells, viral replication was initiated (59). PRRSV-specific neutralizing antibodies. In summary, KU-0063794 this study shown that exosomes can mediate PRRSV transmission and are actually resistant to antibody neutralization, identifying a potential immune evasion mechanism utilized by PRRSV. IMPORTANCE Exosomes have recently been characterized KU-0063794 as bioactive vesicles that function to promote intercellular communication. The exosomes from virally infected cells comprising modified compositions confer several novel functionalities. A study of the secretome of cells infected with PRRSV indicated the exosomal pathway is definitely strongly triggered by PRRSV illness. Here, we demonstrate that PRRSV can use sponsor exosomes to infect naive healthy cells. Furthermore, exosome-mediated viral transmission is largely resistant to PRRSV-specific neutralizing antibodies. Our study provides novel insights into an alternative mechanism of PRRSV transmission that can compromise the host’s anti-PRRSV immune response. (49, 50), and GP5 has been reported to induce apoptosis in bystander cells. Whether the apoptosis induced by GP5 functions through the exosomal pathway requires further study. In addition, PRRSV N protein is a multifunctional nucleolar-cytoplasmic shuttling protein. KU-0063794 Previous studies suggested that PRRSV N protein participates in the modulation of type I interferon and inflammatory reactions (51, 52). Many exosomes derived from virus-infected cells consist of cellular or viral proteins or RNAs that can impact KU-0063794 the gene manifestation or immune response of recipient cells (53,C55). Whether PRRSV N protein modulates innate immune reactions via the exosomal pathway is definitely under investigation in our laboratory. As well as viral proteins, our LC-MS/MS analysis showed that 216 porcine proteins were present in the purified exosomes derived from PRRSV-infected cells, and most of these proteins were identified in the database of exosomes derived from CDKN2A sera of PRRSV-infected pigs inside a earlier study (18). GO analysis showed that these sponsor proteins were associated with cytoskeletal structure, membrane transport, ubiquitin, and response to immune system processes. Viral illness may switch the material of exosomes, and several studies have demonstrated the modified compositions of exosomes derived from virally infected cells confer novel functionalities, such as facilitating viral spread and viral evasion of sponsor cell defenses (56, 57). Our earlier quantitative secretome study also found that approximately 72.4% of secretory proteins that were differentially indicated in PRRSV-infected Marc-145 cells and mock-infected controls were exosomal proteins (17). These differentially indicated exosomal proteins may facilitate viral pathogenesis or sponsor immune response. Unfortunately, we did not quantitatively analyze the material of purified exosomes derived from PRRSV-infected cells with this study. In recent years, the tasks of exosomes released from infected cells have been investigated for a number of viruses, including HIV-1, HCV, hepatitis A disease (HAV), Dengue disease (DENV), human being T-cell lymphotropic disease, the herpesviruses, and severe fever with thrombocytopenia syndrome virus (SFTSV). The findings of these studies suggested the released exosomes consist of viral particles, genomes, mRNAs, microRNAs (miRNAs), or proteins that perform important tasks in viral replication, pathogenesis, and transmission. For example, purified exosomes isolated from HCV- or HAV-infected cells were shown to contain total viral particles and were capable of transmitting illness to naive cells (58). Cells infected with SFTSV also released exosomes comprising virions, and when the exosomes were taken up by uninfected cells, viral replication was initiated (59). Epstein-Barr disease (EBV)-positive tumors secrete exosomes comprising the viral protein latent membrane protein 1 (LMP1), which has inhibitory effects on immune reactions, facilitating immune evasion (60). Some miRNAs encoded by Kaposi’s.