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Zoonotic Spillover in West Bengal: Fruit Bats Serve as Nipah Virus Vector in 2026 Outbreak

Digital artwork features a bat above a red dot on India's map. Lines connect to virus shapes and the year "2026" on a gradient background.

Abstract

The reappearance of the Nipah virus (NiV) in West Bengal, India, in January 2026 marks a significant epidemiological event, breaking a nineteen-year period of relative silence in the eastern region of the subcontinent. This report provides an exhaustive examination of the outbreak, contextualizing it within the broader history of Henipavirus emergence. We analyze the specific virological characteristics of the Bangladesh/India strain (NiV-B), contrasting its transmission dynamics—driven by respiratory spread and renal shedding—with the Malaysian strain (NiV-M). The report delves into the molecular machinery of viral entry, detailing the conformational cascades of the Attachment (G) and Fusion (F) glycoproteins that facilitate the infection of endothelial and neuronal cells. Furthermore, we explore the ecological determinants of spillover, specifically the nexus of the Indian Flying Fox (Pteropus medius) bat ecology, winter climatic conditions, and the cultural practice of date palm sap consumption. Finally, we assess the current state of therapeutic interventions, highlighting the indigenous development of monoclonal antibodies like m102.4 by the Indian Council of Medical Research (ICMR) and the critical challenges of One Health surveillance in high-density populations.

1. Introduction: The Looming Specter of Zoonosis

In the annals of emerging infectious diseases, few pathogens command the same level of immediate dread and scientific fascination as the Nipah virus (NiV). A member of the family Paramyxoviridae and the genus Henipavirus, Nipah virus represents the quintessential zoonotic threat: a pathogen perfectly adapted to its natural reservoir, the fruit bat, yet devastatingly lethal when it crosses the species barrier into humans.1 The virus operates at the volatile intersection of ecology and anthropology, exploiting the subtle encroachments of human agriculture into wildlife habitats to launch sporadic, high-mortality incursions into the human population.

The global medical community first encountered this viral entity in 1998, during an explosive outbreak in Kampung Sungai Nipah, Malaysia. There, the virus utilized domestic pigs as an amplifying host, transforming localized spillover events into a widespread epidemic that devastated the local swine industry and claimed the lives of over 100 pig farmers.3 That initial outbreak established a paradigm of transmission involving an intermediate host. However, as the virus emerged in South Asia—specifically in Bangladesh and India—a new, more direct transmission dynamic became evident. In the Bengal basin, the pig was no longer the necessary bridge; instead, the virus demonstrated the capacity to jump directly from bats to humans, often through contaminated food sources, and subsequently spread from person to person with alarming efficiency.5

In January 2026, the fragility of the human-animal interface was laid bare once again. Health authorities in West Bengal, a state in eastern India, reported a cluster of confirmed Nipah virus cases in the district of North 24 Parganas, near the bustling metropolis of Kolkata.7 This event, occurring nearly two decades after the last confirmed outbreak in the state in 2007, has reignited urgent questions regarding surveillance gaps, viral persistence in reservoir populations, and the resilience of healthcare systems against high-consequence pathogens. Unlike the outbreaks in Kerala, which have occurred with terrifying regularity since 2018, the 2026 West Bengal resurgence serves as a reminder of the virus's "cryptic" nature in the eastern belt—silent for years, yet never truly absent.9

This report aims to deconstruct the 2026 outbreak not merely as a news event, but as a biological and ecological phenomenon. By synthesizing data from the latest epidemiological reports, molecular studies of viral glycoproteins, and ecological surveys of reservoir hosts, we construct a holistic picture of the Nipah virus as it stands in the mid-2020s.

2. The 2026 West Bengal Outbreak: Anatomy of a Resurgence

The resurgence of Nipah virus in West Bengal in early 2026 was not entirely unexpected by virologists, yet its arrival was abrupt and severe. The outbreak provides a contemporary case study of how zoonotic spillover events unfold in densely populated, resource-constrained settings.

2.1. Timeline of Detection and Confirmation

The sequence of events began in the second week of January 2026. On January 11, 2026, samples from two healthcare workers—a male and a female nurse working at a private hospital in Barasat, North 24 Parganas—were flagged for potential viral etiology after they presented with severe, atypical pneumonia and neurological signs.10 These individuals had been caring for a patient who had initially presented with fever and respiratory distress, a common enough presentation in winter that often masks the deadly nature of NiV.11

By January 13, 2026, the suspected cases were confirmed as Nipah virus infection by the Virus Research and Diagnostic Laboratory (VRDL) network. The confirmatory testing was conducted by the All India Institute of Medical Sciences (AIIMS) Kalyani and validated by the National Institute of Virology (NIV) in Pune, the apex body for virological research in India.8 The use of Real-Time Polymerase Chain Reaction (RT-PCR) allowed for the rapid identification of viral RNA in throat swabs and blood samples, a diagnostic speed that contrasts sharply with the delays seen in the 2001 Siliguri outbreak.

As of the latest updates on January 23, 2026, the cluster had expanded to five confirmed cases. This cohort included a doctor, the two initially identified nurses, and another member of the hospital support staff, signaling a significant nosocomial (hospital-acquired) transmission event.7

2.2. Geographic and Demographic Profile

The epicenter of the outbreak, Barasat, serves as a critical junction. Located on the periphery of Kolkata, it represents a "rurban" landscape where urban density meets rural agricultural practices. This interface is ideal for zoonotic spillover, as fruit bats often forage in the orchards and trees that dot the suburban landscape.12

The Nosocomial Pattern: The demographic profile of the 2026 cases is heavily skewed toward healthcare providers. This mirrors the harrowing epidemiology of the 2001 Siliguri outbreak, where 75 percent of cases were hospital staff or visitors.13 The infection of a doctor and multiple nurses suggests that the index patient—the "patient zero" of this cluster—likely had a high viral load in respiratory secretions. In the early stages of the outbreak, before Nipah was suspected, routine care procedures such as nebulization or suctioning likely generated infectious aerosols, exposing staff who were not wearing high-level personal protective equipment (PPE).14

Clinical Status of Patients: The clinical outcomes reported thus far are grave. As of January 23, the female nurse was reported to be in "very critical" condition in the Intensive Care Unit (ICU), requiring ventilator support. The male nurse showed signs of stabilization, but the unpredictability of the disease course—where patients can deteriorate rapidly due to late-onset encephalitis—keeps the prognosis guarded.11

2.3. The Meteorological Catalyst: The January Cold Wave

The timing of the outbreak is inextricably linked to the local climate. January 2026 was marked by a "cold wave" across the Gangetic plains, with minimum temperatures dropping 2–3°C below normal.15 This meteorological context is crucial for two reasons:

  1. Viral Stability: Nipah virus is an enveloped virus that is sensitive to heat and desiccation. Cooler, foggy conditions significantly extend the survival of the virus in the environment, particularly in biological fluids like bat urine or date palm sap.13

  2. Date Palm Sap Harvest: The cold weather coincides with the peak season for harvesting date palm sap (nolen gur). The flow of sap is highest and sweetest during the coldest nights, attracting both human collectors and fruit bats.17

The convergence of these factors created a "perfect storm" for spillover. The low temperatures likely allowed the virus to persist in contaminated sap collected overnight, which was then consumed raw by the index case, initiating the chain of transmission.6

3. Ecological Dynamics: The Reservoir and the Spillover

To understand why Nipah virus re-emerged in 2026, one must look to the skies. The primary reservoir for Nipah virus in South Asia is the Indian Flying Fox, Pteropus medius (formerly Pteropus giganteus). These massive bats, with wingspans of over a meter, play a vital ecological role as seed dispersers and pollinators, but they are also the biological vessels for this deadly pathogen.12

3.1. Pteropus medius: Ecology and Viral Shedding

Pteropus medius populations are widely distributed across India, often roosting in large colonies in banyan or tamarind trees near human settlements. Unlike many other bat species, they do not inhabit caves; they are synanthropic, living among people.20

Viral Shedding Dynamics:

The virus is not constantly shed by infected bats. Instead, shedding is episodic and pulsed. Research indicates that viral shedding—primarily through urine, saliva, and reproductive fluids—is driven by physiological stress.

  • Seasonality: Shedding peaks during the winter months (December to April). This period overlaps with the bats' birthing season and times of nutritional stress due to food scarcity.21 The energy demands of pregnancy and lactation compromise the bats' immune systems, leading to a resurgence of viral replication (recrudescence) and shedding.22

  • Seroprevalence: Surveillance studies conducted in the years leading up to the 2026 outbreak, specifically in West Bengal and Assam, consistently found neutralizing antibodies in bat populations, confirming that the virus circulates continuously within the reservoir.22 However, the actual isolation of viral RNA is rare, making it difficult to predict exactly when a spillover will occur based on bat sampling alone.24

3.2. The Date Palm Sap Pathway

The transmission mechanism in the Bengal basin is distinct from the Malaysian model. In Malaysia, pigs served as the amplifier. In Bengal, the "amplifier" is a clay pot.

The Process of Contamination:

During the winter harvest, sap collectors (gachias) climb date palm trees in the evening to shave the bark and position a clay pot to catch the oozing sap. This sweet, nutrient-rich fluid is irresistible to Pteropus bats.

  • Bat Behavior: Infrared camera studies have captured bats visiting these trees at night. They lick the sap flow, and crucially, they often urinate or defecate while hanging above the pot. The design of the collection system acts as a funnel, capturing bat excreta along with the sap.25

  • Viral Survival: In the cool ambient temperatures of a January night in West Bengal, the virus can survive in the sap for hours or days. The sap is traditionally consumed fresh and raw the next morning as a refreshing drink. It is this specific cultural practice that drives the epidemiology of NiV-B.13

The 2026 investigation is heavily focused on this route. Although no definitive link had been publicly confirmed for the index case by January 23, the seasonal timing strongly implicates date palm sap as the vector.7

3.3. Anthropogenic Pressures and Habitat Loss

The re-emergence of NiV is also a story of habitat fragmentation. Rapid urbanization in districts like North 24 Parganas has reduced the availability of wild fruiting trees. This forces bats to rely more heavily on anthropogenic food sources—orchards and date palm trees—bringing them into closer contact with humans. The "One Health" perspective emphasizes that protecting bat habitats is, paradoxically, a public health measure for humans; healthy, well-fed bats in wild habitats are less likely to shed virus near human homes.12

4. Molecular Virology: The Machinery of Invasion

The pathogenicity of the Nipah virus is encoded in its genome. As a negative-sense RNA virus, its genetic material is antisense to the mRNA required for protein synthesis. The viral genome encodes six structural proteins: Nucleoprotein (N), Phosphoprotein (P), Matrix (M), Fusion (F), Attachment (G), and the Large polymerase (L).1 Among these, the envelope glycoproteins G and F are the architects of infection.

4.1. The G Glycoprotein: The Lock-Picker

The first step in infection is attachment. The Nipah virus G protein is a tetrameric type II membrane protein that protrudes from the viral envelope. Unlike the Hemagglutinin-Neuraminidase (HN) proteins of other paramyxoviruses, the NiV G protein lacks hemagglutinating and neuraminidase activity. Instead, it has evolved to bind with high specificity to members of the Ephrin family of cellular receptors.1

Receptor Specificity:

  • Ephrin-B2: This is the primary receptor. It is ubiquitously expressed on endothelial cells (lining blood vessels) and smooth muscle cells. The high affinity of NiV G for Ephrin-B2 explains the virus's systemic nature and its ability to cause widespread vasculitis.1

  • Ephrin-B3: This receptor is expressed in the brain stem and other neural tissues. Binding to Ephrin-B3 facilitates the virus's entry into the central nervous system (CNS), leading to the severe encephalitis characteristic of the disease.1

Conformational Dynamics: The G protein is not a static hook. Upon binding to the Ephrin receptor, the globular head of the G protein undergoes a series of conformational changes. These shifts physically move the head domains, exposing a previously hidden "stalk" region. This stalk is crucial; it contains the molecular signal that triggers the neighboring F protein.31

4.2. The F Protein: The Fusion Machine

The Fusion (F) protein is the engine of viral entry. It is a class I fusion protein, synthesized as a precursor (F0) that is cleaved by cellular proteases (like cathepsin L) into two subunits, F1 and F2, which remain linked by disulfide bonds. The functional F protein exists as a metastable trimer on the viral surface—a "loaded spring" waiting to be released.19

The Fusion Cascade:

  1. Triggering: When the G protein binds its receptor and exposes its stalk, it interacts with the F protein. This interaction destabilizes the F protein.

  2. Insertion: The F protein undergoes a dramatic refolding. It shoots out a hydrophobic "fusion peptide" from its N-terminus. This peptide acts like a harpoon, embedding itself into the host cell membrane.33

  3. The 6-Helix Bundle (6HB): The extended F protein then collapses back on itself. Regions known as Heptad Repeat A (HRA) and Heptad Repeat B (HRB) zip together to form a highly stable six-helix bundle structure.

  4. Membrane Merger: This zippering action pulls the viral membrane and the host cell membrane together with immense force, overcoming the energy barrier of hydration repulsion. The membranes merge, creating a fusion pore through which the viral ribonucleoprotein complex (vRNP) enters the host cytoplasm.35

Syncytia Formation: Crucially, the F and G proteins are also expressed on the surface of infected host cells. They can interact with Ephrin receptors on neighboring healthy cells, triggering the same fusion process. This leads to the fusion of multiple cells into massive, multi-nucleated giant cells called syncytia. Syncytia formation is a hallmark of Nipah pathology, causing massive tissue disruption and allowing the virus to spread directly from cell to cell, evading neutralizing antibodies in the bloodstream.4

4.3. Immune Evasion Mechanisms

Nipah virus encodes several proteins, particularly the P gene products (P, V, W, and C proteins), that actively dismantle the host's antiviral defenses.

  • Interferon Antagonism: The V and W proteins bind to STAT1 and STAT2, key signaling molecules in the interferon pathway. By sequestering or degrading these proteins, the virus prevents the infected cell from entering an antiviral state or signaling to neighboring cells. This allows the virus to replicate unchecked in the early stages of infection.2

5. Clinical Pathology: The Human Cost

The clinical presentation of Nipah virus infection is a spectrum of severity, heavily influenced by the viral strain (Clade B vs. Clade M) and the route of transmission.

5.1. Incubation and Prodrome

The incubation period is notoriously variable. While the average is 4 to 14 days, outliers of up to 45 days have been documented.3 This variability poses a nightmare for contact tracing, as exposed individuals must be monitored for extended periods.

The prodromal phase mimics a generic viral illness. Patients present with high grade fever, headache, myalgia (muscle pain), sore throat, and vomiting. This non-specific presentation is the "diagnostic trap" that leads to nosocomial spread; until the more specific neurological or respiratory signs appear, the patient is often managed without strict isolation.3

5.2. The Respiratory Syndrome (NiV-B Specificity)

A key differentiator of the Bangladesh/India strain (NiV-B), which is responsible for the 2026 outbreak, is the prominence of respiratory disease. Unlike the Malaysian strain, which was primarily neurotropic, NiV-B causes severe respiratory distress in approximately 70-80% of patients.39

  • Pathology: The virus infects the epithelium of the respiratory tract, causing desquamation and inflammation. This leads to a cough, difficulty breathing, and rapidly progressive atypical pneumonia.

  • ARDS: In severe cases, this progresses to Acute Respiratory Distress Syndrome (ARDS), characterized by widespread inflammation in the lungs, fluid accumulation in the alveoli, and catastrophic failure of oxygenation. This was observed in the "very critical" female nurse in the 2026 West Bengal cluster.11

5.3. Acute Encephalitis

The most feared manifestation is acute encephalitis. The virus breaches the blood-brain barrier (BBB) by infecting the endothelial cells or by retrograde transport along the olfactory nerves.40

  • Symptoms: Clinical signs include dizziness, drowsiness, altered consciousness, and disorientation. This can deteriorate within 24–48 hours into deep coma. Brainstem involvement is common, leading to autonomic dysfunction (fluctuating blood pressure, heart rate variability) and loss of cranial nerve reflexes.37

  • Seizures: Segmental myoclonus (jerking of muscles) and generalized tonic-clonic seizures are frequent. The inflammation of the brain parenchyma leads to cerebral edema (swelling), raising intracranial pressure to lethal levels.

5.4. Long-term Sequelae and Relapse

Nipah virus is unique among acute viral encephalitides in its ability to cause late-onset disease.

  • Relapsing Encephalitis: Survivors of the acute phase can experience a relapse of encephalitis months or years later. This is termed "Late-Onset Nipah Encephalitis." It is believed to be caused by the reactivation of the virus that has persisted in a dormant state within the CNS.40

  • Chronic Neurological Deficits: Even without relapse, approximately 20% of survivors are left with permanent neuropsychiatric sequelae. These include persistent fatigue, personality changes, cognitive decline, and seizure disorders.13 The mechanisms of this persistence are a subject of intense research, with evidence suggesting the virus can hide in neurons or microglia, shielded from the immune system.40

6. Epidemiology: Transmission Dynamics and R0

The transmission dynamics of the 2026 outbreak highlight the duality of Nipah virus spread: inefficient but deadly zoonosis, followed by efficient nosocomial amplification.

6.1. Reproductive Number (R0)

The Basic Reproductive Number (R0) of Nipah virus is generally estimated to be roughly 0.4 to 0.5, meaning that on average, an infected person infects less than one other person. This low R0 is what prevents Nipah from becoming a global pandemic like COVID-19.42

  • Contextual R0: However, the effective reproductive number (Re) can spike significantly in specific settings. In the 2001 Siliguri outbreak, the R0 within the hospital setting was much higher due to the lack of infection control. The 2026 outbreak shows signs of a similar "context-dependent" spike, where a single index case generated at least four secondary cases among healthcare workers.11

  • Superspreading: Nipah transmission is characterized by heterogeneity; most patients do not transmit the virus, but a small number of "superspreaders"—usually those with severe respiratory symptoms—drive the bulk of transmission.43

6.2. Transmission Routes

  • Droplet and Aerosol: The high incidence of respiratory symptoms in NiV-B infections means that coughing generates infectious droplets. While not truly airborne over long distances like Measles, the virus can be aerosolized during medical procedures, posing a severe risk to staff.14

  • Fomites: The virus can survive on surfaces contaminated with respiratory secretions or urine.

  • Direct Contact: Contact with bodily fluids (blood, urine, saliva) is the most efficient route. In previous Kerala outbreaks, transmission occurred through sharing food or sleeping in the same room as the index case.45

6.3. The West Bengal vs. Kerala Pattern

Comparing the epidemiological curves of West Bengal and Kerala reveals a distinct pattern.

  • Kerala: Outbreaks (2018, 2019, 2021, 2023, 2025) are typically smaller and contained more rapidly due to high vigilance. The primary spillover is often ambiguous but linked to bat-infested environments.46

  • West Bengal: Outbreaks (2001, 2007, 2026) are less frequent but tend to be larger and more explosive before detection. The 2001 Siliguri outbreak had 66 cases with a 68% fatality rate. The 2007 Nadia outbreak had 5 cases with 100% fatality. The 2026 outbreak, with 5 cases currently, threatens to follow this high-mortality trajectory if containment fails.48

7. Diagnostics, Therapeutics, and the Quest for a Cure

The high mortality of Nipah virus makes the development of medical countermeasures a priority for the WHO and the Coalition for Epidemic Preparedness Innovations (CEPI).2

7.1. Diagnostic Challenges

Rapid diagnosis is critical but difficult. The virus is a Biosafety Level 4 (BSL-4) pathogen, requiring the highest level of containment for culture.

  • RT-PCR: This is the primary diagnostic tool. It detects viral RNA in throat swabs, nasal swabs, urine, and blood. However, the viral load can be low or intermittent in the early stages, leading to false negatives.

  • Point-of-Care Testing: There is a desperate need for rapid, bedside antigen tests that do not require a BSL-4 or BSL-3 laboratory. Currently, samples must be transported to specialized centers like NIV Pune or AIIMS, adding critical delays.50

7.2. Monoclonal Antibodies: The m102.4 Initiative

The most advanced therapeutic candidate is the monoclonal antibody m102.4.

  • Mechanism: m102.4 is a neutralizing antibody that targets the receptor-binding site on the Nipah G glycoprotein. By occupying this site, it prevents the virus from attaching to the Ephrin-B2/B3 receptors on host cells, effectively neutralizing the virus.51

  • Clinical Use: It has been used on a compassionate basis in previous outbreaks (e.g., Kerala 2018) with some success. It has shown efficacy in protecting African Green Monkeys even when administered days after infection.51

  • Strategic Independence: In December 2025, recognizing the vulnerability of relying on international supplies, the Indian Council of Medical Research (ICMR) re-issued a call for Expression of Interest (EoI) to develop and manufacture monoclonal antibodies indigenously. The goal is to partner with Indian pharmaceutical companies to create a domestic stockpile of m102.4 or similar antibodies, ensuring that treatments are available immediately when an outbreak strikes.52

7.3. Vaccine Landscape

Vaccination remains the long-term goal for prevention.

  • Candidates: Several vaccines are in development. The most prominent are viral vector vaccines (like ChAdOx1 NipahB) and mRNA vaccines. These vaccines express the G or F protein to train the immune system.54

  • Trial Hurdles: The sporadic nature of outbreaks makes traditional Phase 3 clinical trials impossible—there are simply not enough cases to statistically prove efficacy. Therefore, regulators are using the "Animal Rule," allowing approval based on efficacy in animals and safety in humans. Trials for ChAdOx1 NipahB were scheduled to begin in 2026 in endemic regions.54

8. Public Health Response and One Health Strategies

The containment of the 2026 outbreak relies on traditional public health maneuvers executed with extreme rigor.

8.1. Containment Protocols

  • Isolation: The isolation of confirmed cases in negative-pressure rooms is non-negotiable. The Infectious Diseases Hospital in Beleghata, Kolkata, has been designated as the nodal center.11

  • Quarantine: The home quarantine of nearly 100 contacts serves as a "firebreak." These individuals are monitored daily for fever; if symptoms develop, they are immediately isolated and tested.55

  • Contact Tracing: Tracing teams map the movements of the infected individuals, categorized into high-risk (direct physical contact) and low-risk contacts.

8.2. One Health Interventions

The "One Health" approach acknowledges that human health is dependent on animal and environmental health.

  • Ban on Raw Sap: A critical intervention in West Bengal is the ban on the sale and consumption of raw date palm sap in affected districts. Public awareness campaigns urge locals to boil the sap (making gur), which kills the virus, rather than drinking it fresh.26

  • Bat Surveillance: Determining the infection status of local bat colonies can define the risk zone. However, culling bats is not recommended; it is ecologically damaging and can actually increase viral shedding by stressing the population and causing dispersal.56

8.3. Future Outlook

The 2026 outbreak serves as a stress test for India's post-pandemic healthcare infrastructure. While diagnostic capabilities have improved since 2001, the infection of healthcare workers indicates that infection control protocols in peripheral hospitals remain a weak link.

The path forward lies in integrating predictive ecology (monitoring bat stress and climate) with rapid-response clinical trials. The development of indigenous therapeutics like monoclonal antibodies is a strategic imperative. As climate change continues to stress wildlife populations and alter human-animal interfaces, the "spillover" of pathogens like Nipah will likely become more frequent, demanding a vigilance that never sleeps.

Tables and Data Summaries

Table 1: Comparative Analysis of Major Nipah Virus Outbreaks in India

Year

Location

Primary Transmission Route

Key Characteristics

Fatality Rate (Approx.)

2001

Siliguri, West Bengal

Nosocomial (Hospital)

Massive transmission within healthcare facilities; lack of PPE.

~68%

2007

Nadia, West Bengal

Zoonotic / Foodborne

Linked to date palm sap consumption; very high mortality.

100%

2018

Kozhikode, Kerala

Zoonotic -> Nosocomial

Index case infected by bats; subsequent spread in hospitals.

~91%

2026

Barasat/Kolkata, WB

Nosocomial

Re-emergence after 19 years; multiple HCWs infected; winter onset.

TBD (Critical cases)

Table 2: Molecular Functions of Nipah Virus Glycoproteins

Protein

Full Name

Primary Function

Mechanism of Action

Therapeutic Target

G

Attachment Glycoprotein

Receptor Binding

Binds to Ephrin-B2 (endothelium/neurons) and Ephrin-B3. Triggers conformational change in F.

Target of m102.4 monoclonal antibody.

F

Fusion Glycoprotein

Membrane Fusion

Exists in metastable pre-fusion state. Upon triggering, inserts fusion peptide and zips into 6-Helix Bundle, merging membranes.

Target of fusion inhibitors and peptide drugs.

Table 3: Clinical Phases of Nipah Virus Infection (NiV-B Strain)

Phase

Timeline

Symptoms

Pathological Basis

Incubation

4-14 Days (up to 45)

None (Asymptomatic)

Viral replication in initial entry site (oropharynx/lungs).

Prodrome

Days 1-3 of illness

Fever, Headache, Myalgia, Vomiting

Systemic viremia; cytokine response.

Respiratory

Days 3-7

Cough, Dyspnea, Atypical Pneumonia, ARDS

Viral replication in lung epithelium; vasculitis in pulmonary vessels.

Encephalitic

Days 5+

Dizziness, Confusion, Seizures, Coma

Invasion of CNS; inflammation of brain parenchyma and brainstem.

Late Sequelae

Months/Years later

Relapsing Encephalitis, Convulsions

Reactivation of dormant virus in CNS (mechanism unclear).

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