Respiratory syncytial virus (RSV) is the most common pathogen causing viral pneumonia in children. RSV usually occurs in neonates and infants less than 6 months old, but also occurs in immunocompromised and elderly people. RSV is transmitted by air droplets and close contact. Infants shortly after birth may be infected with RSV as maternal antibodies cannot prevent infection. RSV reinfection is extremely common since antibodies also cannot completely prevent infection, with a reinfection rate of up to 65% within 10 years. However, no effective RSV vaccine has been developed for the past 50 years. The RSVF protein is highly conserved, functions to promote fusion of the virus with host cells, and is also a primary target for neutralizing antibodies.
RSF belongs to the family paramyxoviridae and the genus pneumoviruses, including subpopulations A and B. The RSF is highly conserved among RSV isolates with high amino acid sequence homology. The 04-2H10 chimeric antibody is superior to MEDI8897 and Palivizumab in neutralizing subtype A RSV pseudovirus infection.
Mechanism of Action
Respiratory syncytial virus (RSV, which also belongs to the family paramyxoviridae) is the most common cause of viral pneumonia in children. Currently, there is no safe rsv vaccine and no effective treatment.)
RSV causes cells to produce devastating reactive oxygen species (ros) molecules that drive cells to release signals to and overreact to the immune system, producing inflammatory responses similar to asthma attacks, which far outweigh the injury caused by the virus itself.
Recent studies have shown that cytokines and chemokines were essential in the pathogenesis of RSV infectious diseases and immune responses, Th1- and Th2 cytokine patterns determine the types of immune responses against RSV infection, and cytokine expression profile affects the pathogenesis and chronicity of RSV. Therefore, understanding the regulatory mechanism of cytokine expression in RSV infection is favorable to take preventive measures to control the occurrence and development of RSV diseases. Effects of cytokines and chemokines in the response against RSV infection are discussed herein, as well as the potential effects of the suppressor of cytokine signaling (SOCS) proteins on regulating these immune responses.
Clinical Study for RSV
YH009 is currently in the CMC preparation phase.