Nipah virus (NiV) is a highly lethal zoonotic paramyxovirus that emerged in Malaysia in 1998. It is a human pathogen capable of causing severe respiratory infection and encephalitis. The natural reservoir of NiV, Pteropus fruit bats, remains a continuous virus source for future outbreaks, although infection in the bats is largely asymptomatic. NiV provokes serious disease in various mammalian species. In the recent human NiV outbreaks in Bangladesh and India, both bats-to-human and human-to-human transmissions have been observed. NiV has been demonstrated to interfere with the innate immune response via interferon type I signaling, promoting viral dissemination and preventing antiviral response. Studies of humoral immunity in infected NiV patients and animal models have shown that NiV-specific antibodies were produced upon infection and were protective. Studies on cellular immunity response to NiV infection in human and animal models also found that the adaptive immune response, specifically CD4+ and CD8+ T cells, was stimulated upon NiV infection. The experimental vaccines and therapeutic strategies developed have provided insights into the immunological requirements for the development of successful medical countermeasures against NiV. This review summarizes the current understanding of NiV pathogenesis and innate and adaptive immune responses induced upon infection.

To evaluate the long-term humoral immune response to Nipah virus (NiV) in a cohort of 25 survivors after 25 years of post-infection. A total of 25 survivors of NiV infection from the 1998 outbreak were recruited for sample collection. The serum IgG antibody response to NiV antigens, specifically nucleocapsid (N), fusion glycoprotein (F) and attachment glycoprotein (G) was evaluated using ELISA. Additionally, the samples were tested for neutralizing antibodies and memory B cell responses. Detection rates of anti-NiV-F and anti-NiV-G were 56% and 60%, respectively, among the survivors at a 1:100 dilution, whereas only 20% were specifically reactive to rNiV-N. Notably, all samples that tested positive for NiV-F and NiV-G at this dilution also exhibited neutralizing antibodies, highlighting the specificity of these assays. Live virus neutralization assay showed that 72% of survivors had detectable neutralizing antibodies, with varying titers, indicating long-lasting immune memory. Furthermore, memory B cell responses specific to NiV-F and NiV-G were observed in six randomly selected survivors, suggesting the presence of enduring immunological memory. These findings highlight the potential of NiV-F and NiV-G as reliable markers for NiV exposure and underscore the need for continuous surveillance and research. Such efforts are crucial for advancing vaccine development and improving preparedness for future NiV outbreaks.