Introduction

The Nipah virus (NiV) represents one of the most significant viral threats to global health security. Classified within the family Paramyxoviridae and genus Henipavirus, NiV is an emerging zoonotic pathogen known for its high case fatality rate, broad host range, and ability to transmit between humans, Due to its epidemic potential and the lack of licensed vaccines or therapeutics, the World Health Organization (WHO) has designated NiV as a priority pathogen requiring urgent research and development (R&D) action,. Recent outbreaks in South Asia during 2025 and 2026 have renewed global urgency to understand the virus’s ecology and accelerate the development of medical countermeasures.

Origins, Virology, and Diversity

Nipah virus was first recognized following a major outbreak of severe encephalitis among pig farmers in Malaysia and Singapore in 1998 and 1999. The virus was named after Sungai Nipah, the Malaysian village where the virus was first isolated from a patient. That initial outbreak resulted in 265 human cases with 105 deaths in Malaysia and led to the culling of over one million pigs to contain the spread.

The virus possesses a single-stranded, negative-sense RNA genome, approximately 18kb in length, encoding six structural proteins: nucleocapsid (N), phosphoprotein (P), matrix (M), fusion (F), glycoprotein (G), and large polymerase (L). The G protein binds to cellular receptors Ephrin-B2 and Ephrin-B3, which are highly conserved across mammals, explaining the virus’s ability to infect a wide variety of species, including humans, pigs, horses, dogs, and cats.

Genomic sequencing has identified two distinct viral clades:

1. The Malaysia Genotype (NiV-M): Responsible for the 1998–1999 outbreaks, this strain predominantly causes neurological symptoms and utilizes pigs as an intermediate amplifying host.
2. The Bangladesh/India Genotype (NiV-B): This strain, circulating in South Asia, is associated with a higher case fatality rate (often exceeding 70%) and a higher prevalence of respiratory symptoms alongside encephalitis. Crucially, the NiV-B strain is more frequently associated with human-to-human transmission,

Ecological Reservoir and Transmission Dynamics

The natural reservoir for NiV is fruit bats of the family Pteropodidae, specifically the genus Pteropus (flying foxes). These bats are endemic across South and Southeast Asia, Australia, and parts of Africa, a geographic range that puts more than 2 billion people at potential risk of spillover. The virus does not appear to cause disease in bats, but they shed it in saliva, urine, and excreta.

Zoonotic Spillover

Transmission to humans occurs through two primary zoonotic pathways:

1. Intermediate Hosts: In the Malaysian outbreak, bats transmitted the virus to pigs (likely via fruit dropped into pigsties), which amplified the virus and infected farmers through direct contact with respiratory secretions and fluids.
2. Foodborne Transmission: In Bangladesh and India, the primary route of spillover is the consumption of raw date palm sap (tari) or fruit contaminated with bat urine or saliva. Bats often lick the sap streams as they flow into collection pots on trees. The virus can survive in sugar-rich solutions like date palm sap for roughly 7 days at 22°C.

Human-to-Human Transmission

Once a human is infected, the virus can spread person-to-person. This occurs primarily through close contact with the body fluids (blood, urine, saliva) or respiratory secretions of an infected patient. This mode of transmission is particularly concerning in healthcare settings (nosocomial transmission) and among family caregivers. While the virus is not considered highly airborne like measles, transmission via respiratory droplets occurs, and virus-laden aerosols can remain viable for up to 90 minutes.

Pathogenesis

1. Entry and Targeting: NiV enters the respiratory tract through the oronasopharyngeal route. It targets the respiratory epithelium primarily.
2. Cellular mechanisms and viral replication: A characteristic of the NiV infection is the formation of syncytial giant cells and severe tissue damage triggered by cell fusion and replication. The NiV G (attachment) and F (fusion) proteins bind to ephrin-B2/B3 receptors in cells, which facilitates their entry into them.
3. Virus Systematic Spread: After initial replication, the virus spreads through the bloodstream to target organs, primarily through the endothelial cells of small blood vessels.
4. Major pathology

• CNS: Nipah virus (NiV) can infiltrate the brain via two primary pathways: the hematogenous route, where the virus replicates within endothelial cells, leading to a breach of the blood-brain barrier (BBB), and Direct entry via the olfactory nerve that travels from the nasal cavity to the olfactory bulb through the cribriform plate.
• Respiratory: An atypical pneumonia-like illness characterized by rapid-onset distress and severe respiratory problems.

5. Strategies of Immune Evasion: A high-level replication is enabled by STAT inhibition, IFN suppression, hindering T-cell recognition, and delaying the adaptive immune response of the host by NiV
6. Disease progression: In the first 10 days after symptoms begin, RNA from the virus is detectable in throat swabs and blood, followed by detection in cerebrospinal fluid, indicating progressive CNS invasion.

Epidemiology: The 2025–2026 Situation

While no new outbreaks have occurred in Malaysia or Singapore since 1999, Bangladesh and India experience almost annual outbreaks.

Bangladesh (2025)

Between January and August 2025, Bangladesh reported four fatal cases of NiV infection across three divisions. Unlike typical seasonal patterns (December to May), one case in August 2025 occurred in the Naogaon district, marking an unusual “off-season” transmission event where the patient had no history of consuming raw date palm sap. This temporal and geographic expansion suggests the epidemiology of the virus may be evolving, posing a year-round threat. To date, Bangladesh has recorded 347 cases with a cumulative fatality rate of 71.7%.

India (2025–2026)

India has seen sporadic outbreaks, notably in Kerala and West Bengal. In July 2025, an outbreak in Kerala’s Palakkad and Malappuram districts resulted in two deaths among three cases.

More recently, in January 2026, the virus re-emerged in West Bengal. On January 26, 2026, Indian authorities notified the WHO of two confirmed cases in Barasat (North 24 Parganas district). Both patients were young healthcare workers (nurses) at a private hospital who developed symptoms in late December 2025. This cluster marks the third recorded outbreak in West Bengal (previous events occurred in 2001 and 2007). As of late January 2026, extensive contact tracing of over 190 individuals yielded negative results, indicating the cluster had not spread further into the community.

Regional Alert

The resurgence has triggered heightened surveillance across Asia. In January 2026, Thailand began screening passengers arriving from West Bengal, and Nepal implemented health desks at its borders and international airport to screen for symptoms, given the proximity of West Bengal to Nepal’s eastern border.

Clinical Presentation and Diagnosis

Signs and Symptoms The incubation period for NiV typically ranges from 4 to 14 days, though it can extend up to 45 days, complicating quarantine efforts.

• Prodromal Phase: Illness usually begins with non-specific flu-like symptoms, including fever, headache, myalgia (muscle pain), vomiting, and sore throat.
• Acute Phase: The disease can progress rapidly to dizziness, drowsiness, and altered consciousness, signaling acute encephalitis (brain swelling). Severe cases may suffer seizures and progress to coma within 24 to 48 hours.
• Respiratory Involvement: Atypical pneumonia and acute respiratory distress syndrome (ARDS) are frequently observed, particularly in patients infected with the Bangladesh/India strain.
• Sequelae: Approximately 20% of survivors suffer long-term neurological consequences, such as seizure disorders and personality changes. A small subset may experience relapsing encephalitis months or years after the initial infection.

Diagnostics

Early diagnosis is challenging due to non-specific early symptoms. Definitive diagnosis relies on Real-Time Polymerase Chain Reaction (RT-PCR) testing of throat swabs, urine, blood, and cerebrospinal fluid (CSF) during the acute phase. Later in the disease course or convalescence, Enzyme-Linked Immunosorbent Assay (ELISA) is used to detect antibodies. Because NiV is a Biosafety Level 4 (BSL-4) pathogen, handling live virus samples requires maximum containment facilities.

Therapeutics and Vaccines: R&D Progress

Currently, there are no licensed treatments or vaccines for Nipah virus infection; clinical management is limited to intensive supportive care. However, significant strides have been made in the R&D pipeline as of 2026.

Vaccine Candidates

• ChAdOx1 NipahB: In a major milestone, the University of Oxford launched the world’s first Phase II clinical trial for its Nipah vaccine in December 2025. This trial is taking place in Bangladesh, enrolling 306 healthy participants. The vaccine uses the same viral vector platform as the AstraZeneca COVID-19 vaccine.
• HeV-sG: A subunit vaccine originally developed for Hendra virus has shown cross-protection against NiV in animal models and is currently licensed for use in horses in Australia. In a study funded by Coalition for Epidemic Preparedness Innovations (CEPI), results published in The Lancet (Dec 2025/Jan 2026) confirmed the vaccine’s safety and well-tolerance. One dose produced some response in the study of 192 healthy adults, but two doses (specifically 100 g doses given 28 days apart) produced the strongest neutralizing antibody levels against both Bangladesh and Malaysia strains of Nipah.
• Investigational Stockpiles: The Coalition for Epidemic Preparedness Innovations (CEPI) and the Serum Institute of India are collaborating to manufacture an investigational reserve of up to 100,000 vaccine doses for emergency deployment.

Therapeutics

• Monoclonal Antibodies (mAbs): The m102.4 antibody has completed Phase 1 clinical trials and has been accessed for compassionate use. Another candidate, MBP1F5, is scheduled to begin clinical trials in 2026. These antibodies target the viral G glycoprotein to neutralize the virus.
• Antivirals: Remdesivir has shown efficacy in non-human primates when administered as post-exposure prophylaxis, reducing disease severity. Ribavirin was used in the 1999 Malaysia outbreak, but its efficacy remains unclear.

Prevention and Infection Control

In the absence of pharmaceutical cures, prevention remains the primary defense against NiV.

Community and Zoonotic Prevention

• Date Palm Sap: Interventions focus on preventing bats from accessing sap collection pots using bamboo skirts or other physical barriers. Public health messages emphasize that raw date palm sap should not be consumed; it must be boiled to destroy the virus.
• Animal Handling: Strict biosecurity is required on pig farms. Suspected infected animals must be culled, and handlers must wear protective clothing. Fruits found on the ground or showing signs of animal bites should be discarded.

Healthcare Infection Prevention and Control (IPC)

Human-to-human transmission is a major driver of outbreaks in India and Bangladesh. Hospitals must implement strict protocols:

• Isolation: Suspected cases should be isolated in negative-pressure rooms if possible.
• PPE: Healthcare workers must use standard, contact, and droplet precautions. Because the virus can be aerosolized during certain medical procedures (and potentially through severe coughing), the use of N95 respirators (or higher), eye protection, gowns, and gloves is recommended for all patient care.
• Sanitation: Regular hand hygiene and disinfection of surfaces with hospital-grade disinfectants (e.g., sodium hypochlorite) are essential, as the virus can survive on surfaces.

Conclusion

The Nipah virus remains a formidable pathogen with the capacity to cause severe morbidity and mortality due to late diagnosis, absence of specific antiviral agents, and insufficient care. The outbreaks in 2025 and 2026 highlight the virus’s persistent threat and the evolving nature of its transmission, including off-season spillover events and nosocomial clusters. While the immediate risk of a global pandemic is currently assessed as low by the WHO, the virus’s high lethality and lack of licensed countermeasures necessitate continued vigilance. The initiation of Phase II vaccine trials in Bangladesh marks a historic step forward, offering hope that a preventive tool may soon be available to protect vulnerable populations in endemic regions. Until then, rigorous surveillance, public awareness regarding raw date palm sap, and robust infection control in hospitals remain the world’s most effective tools against the Nipah virus. Since there is no precise approved vaccine or medication, the “Benchmark” treatment includes intensive, high-quality supportive care for the management of acute respiratory and neurological complications.

यस विषयबारे विस्तृतमा सुन्नुहोस् : नेपाली भाषामा