Zika Virus

Table of Contents

  1. Overview
  2. Epidemiology and 2016 Outbreak
  3. Virology and Pathophysiology
  4. Transmission Routes
  5. Clinical Presentation
  6. Congenital Zika Syndrome
  7. Guillain-Barré Association
  8. Diagnosis
  9. Treatment and Management
  10. Prevention and Travel Advisories
  11. Prognosis
  12. Recent Research
  13. References
  14. Featured Videos

Overview

Zika virus (ZIKV) is a member of the family Flaviviridae, genus Flavivirus. It is a single-stranded, positive-sense RNA virus with an enveloped virion displaying icosahedral symmetry. Its genome is approximately 10.8 kilobases in length and encodes four structural proteins — capsid (C), precursor membrane (prM), envelope (E) — and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5) essential for replication and immune evasion.

ZIKV was first isolated in April 1947 from a febrile sentinel Rhesus macaque housed in a cage in the Zika Forest of Uganda — a study conducted by the Yellow Fever Research Institute. The virus takes its name from this forest. The first documented human infections occurred in Nigeria in 1952. For decades, ZIKV circulated at low endemic levels across equatorial Africa and Asia, causing only sporadic, mild human illness.

The virus gained global attention during the 2015–2016 epidemic in the Americas when it was linked to two devastating complications previously unrecognized for this pathogen: a sharp rise in microcephaly and other severe fetal brain malformations (collectively termed Congenital Zika Syndrome), and an increase in cases of Guillain-Barré syndrome (GBS). These associations prompted the World Health Organization to declare a Public Health Emergency of International Concern (PHEIC) in February 2016.

Approximately 80% of ZIKV infections are asymptomatic. When symptomatic, illness is typically mild and self-limiting, lasting 2–7 days. However, ZIKV is unique among arboviruses for two reasons: it is the only arbovirus with confirmed sexual transmission, and it is a potent teratogen capable of crossing the placenta and causing catastrophic fetal neurodevelopmental injury throughout pregnancy. As of 2024, no approved antiviral treatment or preventive vaccine exists.

Epidemiology and 2016 Outbreak

Following its 1947 discovery, ZIKV remained largely confined to sub-Saharan Africa and equatorial Asia. Serological surveys confirmed low-level human exposure across Nigeria, Uganda, Tanzania, India, Malaysia, and Indonesia, but clinically recognized outbreaks were rare. The first well-documented outbreak outside Africa/Asia occurred on Yap Island (Federated States of Micronesia) in 2007, affecting approximately 73% of the island's population of 11,250 — the vast majority experiencing only mild illness with no deaths or hospitalizations reported at the time.

The 2013–2014 outbreak in French Polynesia (estimated 28,000 cases, roughly 11% of the population) was the critical turning point. It was during this outbreak that epidemiologists first identified a statistically significant association between ZIKV infection and Guillain-Barré syndrome — an observation that would prove prescient.

Brazil first reported an unusual cluster of illness with rash in the northeast states of Bahia and Rio Grande do Norte in early 2015, confirmed as ZIKV by May 2015. By October 2015, Brazilian health authorities noted a dramatic increase in newborns with microcephaly in the northeast — a region experiencing intense ZIKV transmission. The association was formally reported to the WHO in November 2015, and a PHEIC was declared on February 1, 2016.

The 2015–2016 epidemic spread to 87 countries and territories across the Americas, Southeast Asia, and the Pacific. Brazil bore the greatest burden, with an estimated 1.5 million ZIKV infections. Brazil confirmed 2,823 cases of microcephaly — approximately 10 times the pre-epidemic baseline rate. Across the Americas, an estimated 700,000 symptomatic ZIKV cases were reported during 2016, though the true burden (accounting for asymptomatic cases) was far higher.

In the United States, 5,168 ZIKV cases were reported in 2016: 4,897 travel-associated and 224 locally acquired (213 in Florida, 6 in Texas, 5 in other states via mosquito transmission). Among US cases, 1,306 occurred in pregnant women. The epidemic largely subsided after 2017 as population immunity built up across affected regions, though endemic transmission continues in parts of tropical Latin America, Southeast Asia, and the Pacific Islands.

Virology and Pathophysiology

ZIKV belongs to the Flaviviridae family and is phylogenetically related to dengue virus, West Nile virus, yellow fever virus, and Japanese encephalitis virus — all transmitted by arthropod vectors. Two ZIKV lineages are recognized: an African lineage (represented by the prototype MR766 strain) and an Asian lineage. The Asian lineage seeded the Yap Island, French Polynesia, and ultimately the Americas epidemic, and it is this lineage associated with congenital Zika syndrome.

The mosquito-to-human transmission cycle begins when a female Aedes mosquito takes a blood meal from a viremic host. The virus replicates in the mosquito's midgut epithelium over an extrinsic incubation period of approximately 10–14 days, then disseminates to the salivary glands. Upon the mosquito's next blood meal, ZIKV is inoculated into the dermis of the new human host in infectious saliva.

Following skin inoculation, ZIKV preferentially targets epidermal dendritic cells — specifically Langerhans cells — which express the C-type lectin DC-SIGN and AXL receptor tyrosine kinase, both used by ZIKV for entry. The virus disseminates via lymphatics to regional lymph nodes and subsequently enters the bloodstream, producing viremia that typically persists 3–12 days post-exposure (the intrinsic incubation period is generally 3–14 days).

Neurotropism and teratogenicity: The most clinically significant aspect of ZIKV pathophysiology is its ability to cross the blood-brain barrier and infect neural progenitor cells (NPCs) in the fetal developing brain. ZIKV binds to the AXL receptor tyrosine kinase, which is highly expressed on cortical NPCs, particularly during first-trimester neurogenesis. Infection of NPCs triggers apoptosis (programmed cell death), cell cycle arrest, mitotic spindle disruption, and dysregulated gene expression — resulting in dramatically reduced neuronal proliferation. Since neuronal number is determined primarily during first-trimester neurogenesis, early infection produces the most severe cortical underdevelopment and microcephaly.

Immune evasion: The ZIKV NS5 protein specifically antagonizes STAT2 phosphorylation, thereby blocking type I interferon (IFN-α/β) signaling — a major innate antiviral defense mechanism. This allows sustained viral replication particularly in interferon-responsive neural tissues.

Placental and genital tropism: Placental transmission is facilitated by ZIKV's ability to infect Hofbauer cells (placental macrophages) and cytotrophoblasts — cells that express AXL and TIM-1 entry receptors. The placental barrier, particularly robust in the third trimester, offers incomplete protection — especially in the first trimester when the placenta is least mature. In the male reproductive tract, ZIKV replicates in testicular Sertoli cells (blood-testis barrier immune privilege), enabling persistence in semen for weeks to months after resolution of systemic illness.

Transmission Routes

Mosquito-borne (primary route): The primary vector is Aedes aegypti, the urban yellow fever mosquito, which bites predominantly during the day (peak activity at dawn and dusk). Aedes albopictus (the Asian tiger mosquito) is a secondary, competent vector with a broader geographic range extending into temperate climates — raising concern for northward spread of ZIKV in a warming climate. Both species breed in small, standing water containers in and around human habitations.

Sexual transmission — a unique feature: ZIKV is the only known arbovirus with confirmed person-to-person sexual transmission. Documented routes include male-to-female (most common), female-to-male, and male-to-male transmission. ZIKV RNA has been detected in semen, vaginal secretions, saliva, blood, urine, and breast milk. The critical issue for public health is that sexually active partners of returned travelers can contract ZIKV without any mosquito exposure, including pregnant women whose partners traveled to affected areas.

Maternal-fetal (vertical) transmission: ZIKV can be transmitted from a pregnant woman to her fetus at any point during pregnancy through the placenta (transplacental) or potentially during delivery (intrapartum). First-trimester infection carries the highest risk of severe Congenital Zika Syndrome, but fetal brain abnormalities have been documented following infection in all three trimesters. The proportion of infected pregnant women whose fetuses develop detectable abnormalities ranges from approximately 5–42% depending on the study, timing of infection, and imaging sensitivity.

Blood transfusion and organ transplantation: ZIKV transmission via blood transfusion was documented during the French Polynesia outbreak, and ZIKV RNA has been detected in blood donations from asymptomatic donors. In the US and other affected countries, nucleic acid testing (NAT) of blood donations is implemented in endemic periods. Transmission via solid organ transplantation has also been reported.

Routes NOT documented for transmission: ZIKV is not transmitted by casual contact, respiratory droplets, intact skin contact, or — based on available evidence — breastfeeding. Although ZIKV RNA has been detected in breast milk, no infant transmission through breastfeeding has been confirmed, and the WHO advises that the benefits of breastfeeding outweigh theoretical risks; continued breastfeeding is recommended in affected areas.

Clinical Presentation

The striking epidemiological fact about ZIKV infection is that approximately 80% of infected persons remain entirely asymptomatic. This high rate of subclinical infection contributed to the rapid, largely undetected spread of ZIKV across the Americas in 2015–2016 and complicates control efforts.

When symptomatic disease occurs, it is typically mild and self-limiting, with a duration of 2–7 days. The illness rarely requires hospitalization in otherwise healthy adults. The incubation period from mosquito bite to symptom onset is generally 3–14 days (most commonly 3–7 days).

Classic clinical tetrad of symptomatic ZIKV disease:

  1. Low-grade fever: Temperature typically 37.8–38.5°C (100–101.3°F); rarely exceeds 39°C — notably lower than dengue fever's characteristic high fever.
  2. Maculopapular rash: Present in over 90% of symptomatic cases; begins on the face and spreads centrifugally to the trunk and extremities; often pruritic (itchy) in approximately 50% of patients; may appear within hours of fever onset. The rash is a key distinguishing feature from dengue, where rash timing differs.
  3. Arthralgia: Joint pain, predominantly affecting the small joints of the hands and feet; typically symmetric; may be accompanied by mild periarticular edema. Less severe than chikungunya arthralgia, which is characteristically debilitating.
  4. Non-purulent conjunctivitis: Bilateral conjunctival injection (red eyes) without discharge; present in approximately 55% of symptomatic cases — another useful distinguishing feature from dengue.

Additional symptoms may include myalgia, headache, retro-orbital pain (pain behind the eyes), peripheral edema, and malaise.

Differential diagnosis is critical in endemic regions: dengue fever presents with higher fever, more severe myalgia and headache, thrombocytopenia, and risk of hemorrhagic complications — none of which are characteristic of ZIKV. Chikungunya is distinguished by its severe, often incapacitating polyarthralgia. Rubella, measles, and other viral exanthems may mimic ZIKV rash. In endemic areas, co-infection with dengue and ZIKV has been documented, which complicates clinical diagnosis.

Serious illness from ZIKV in otherwise healthy adults is uncommon. However, immunocompromised individuals, elderly patients, and those with comorbidities may experience more severe or prolonged disease. The most feared complications — Guillain-Barré syndrome and congenital malformations — are post-infectious phenomena, not manifestations of acute viral illness severity.

Congenital Zika Syndrome

The recognition of Congenital Zika Syndrome (CZS) in 2015–2016 fundamentally changed the medical world's understanding of ZIKV. Previously considered a mild, inconsequential arboviral illness, ZIKV was revealed as one of the most potent known human teratogens — capable of catastrophic fetal brain injury when infection occurs during pregnancy.

Microcephaly: The most publicized manifestation of CZS. Defined clinically as a head circumference more than 2 standard deviations (SD) below the mean for gestational age and sex; severe microcephaly is defined as more than 3 SD below the mean. ZIKV-associated microcephaly frequently falls into the severe category. Microcephaly reflects profoundly reduced brain growth — primarily from destruction and failure of proliferation of neural progenitor cells during cortical neurogenesis.

Congenital Zika Syndrome — the full constellation: CZS encompasses a broader spectrum of abnormalities beyond microcephaly alone:

Risk by trimester: First-trimester infection carries the highest risk of severe CZS. Some series estimate that approximately 6–12% of first-trimester ZIKV infections result in detectable fetal abnormalities, though rates vary widely by study design and imaging sensitivity. Importantly, second- and third-trimester infections can also cause fetal brain abnormalities — no trimester confers complete protection.

Long-term outcomes: Children born with severe CZS (particularly those with severe microcephaly, extensive cortical malformations, and ventriculomegaly) face profound neurodevelopmental impairment: cognitive disability, severe motor dysfunction, feeding difficulties requiring gastrostomy tube placement, refractory seizure disorders, and hearing and vision impairment. These children require lifelong multidisciplinary care and represent an enormous burden on families and healthcare systems.

Late-onset CZS ("slow CZS"): A particularly sobering finding from longitudinal Brazilian cohort studies is that some infants born with normal or near-normal head circumference — and thus initially reassuring ultrasound findings — subsequently develop postnatal microcephaly and neurodevelopmental regression during the first year of life. This "late-onset" or "slow" CZS underscores the critical need for long-term neurodevelopmental follow-up of all ZIKV-exposed pregnancies, not only those with abnormal prenatal imaging.

Guillain-Barré Association

The association between ZIKV and Guillain-Barré syndrome (GBS) was first detected during the 2013–2014 French Polynesia outbreak, where a 20-fold increase in GBS incidence was observed concurrent with ZIKV transmission. This association was subsequently confirmed across multiple ZIKV-affected countries during the 2016 epidemic. The estimated risk of GBS following ZIKV infection is approximately 1 in 4,000 infections — making it a rare but important complication given the large number of ZIKV infections during the epidemic.

Mechanism: ZIKV-associated GBS is a post-infectious, immune-mediated polyneuropathy. The leading mechanistic hypothesis is molecular mimicry — ZIKV antigens share structural epitopes with gangliosides present in peripheral myelin and neuronal membranes. The immune response mounted against ZIKV inadvertently attacks peripheral nerves, producing demyelination and/or axonal injury. The timing of GBS onset — typically 2–4 weeks after acute ZIKV infection — is consistent with this post-infectious, autoimmune mechanism.

Clinical features of ZIKV-associated GBS: The predominant pattern is acute inflammatory demyelinating polyneuropathy (AIDP), the most common GBS subtype globally. Patients present with ascending flaccid paralysis, areflexia, and variable sensory symptoms. In several ZIKV-GBS series, cranial nerve involvement (facial diplegia, dysphagia) was more frequent than in classic post-Campylobacter GBS. Respiratory muscle weakness necessitating mechanical ventilation occurs in approximately 18% of ZIKV-GBS cases. Most patients reach peak disability within 4 weeks of symptom onset.

Treatment: ZIKV-associated GBS is treated with standard GBS protocols: intravenous immunoglobulin (IVIG) at 2 g/kg over 2–5 days, or plasmapheresis (plasma exchange). Both are equally effective; they are not additive and should not be combined. Corticosteroids are not beneficial in GBS and are not recommended. ICU monitoring for respiratory failure, autonomic instability, and deep vein thrombosis prophylaxis are standard supportive measures.

Prognosis: The majority of ZIKV-GBS patients recover fully or near-fully over weeks to months. However, recovery can be prolonged, and approximately 5% of GBS patients overall (including ZIKV-associated cases) have residual disability at 12 months. Death from GBS complications (respiratory failure, autonomic instability, pulmonary embolism) occurs in approximately 3–5% of cases in adequately resourced settings.

Diagnosis

Accurate ZIKV diagnosis is challenging due to: the high proportion of asymptomatic infections, overlapping clinical features with dengue and chikungunya, and significant cross-reactivity of ZIKV antibodies with other flaviviruses (particularly dengue and yellow fever) in serological assays. The diagnostic approach depends on the timing of specimen collection relative to symptom onset.

Acute infection (symptoms present for less than 7 days):

Convalescent phase (symptoms present for more than 7 days):

Pregnancy-specific testing protocol (CDC guidance): Any pregnant woman with potential ZIKV exposure (travel to endemic area, or unprotected sexual contact with a partner who traveled) should be tested, even if asymptomatic. For symptomatic pregnant women: simultaneous RT-PCR (serum + urine) and ZIKV IgM serology. For asymptomatic pregnant women with travel exposure: RT-PCR and IgM at first visit, with repeat IgM serology 2–12 weeks after potential exposure.

Fetal and neonatal assessment: For pregnancies with confirmed or probable maternal ZIKV infection, serial fetal ultrasound (every 3–4 weeks) is recommended to monitor for microcephaly, intracranial calcifications, and ventriculomegaly. If fetal abnormalities are detected, amniocentesis for ZIKV RT-PCR can confirm fetal infection, though the clinical management implications of a positive result are limited (no antiviral treatment is available). Neonates born to ZIKV-exposed pregnancies require head ultrasound, ophthalmological evaluation, audiology screening, and long-term neurodevelopmental follow-up regardless of head circumference at birth.

No FDA-cleared, rapid, point-of-care ZIKV diagnostic test has been approved as of 2024, though multiple platforms are under development.

Treatment and Management

There is no approved antiviral treatment for Zika virus disease as of 2024. Management is entirely supportive, focused on symptom relief in the acute phase and comprehensive surveillance and multidisciplinary care in pregnant women and ZIKV-exposed neonates.

Acute illness management (adults):

Pregnancy management: A confirmed or probable ZIKV-exposed pregnancy warrants multidisciplinary care involving maternal-fetal medicine (MFM), infectious disease, neonatology, neurology, and social work. Key components include:

Neonatal evaluation (all ZIKV-exposed pregnancies): Head ultrasound (or MRI if abnormalities suspected), ophthalmological exam, automated auditory brainstem response (AABR) hearing screen, developmental milestone monitoring through at least age 3 years, and referral to early intervention programs.

GBS management: IVIG (2 g/kg over 2–5 days) or plasmapheresis; ICU admission if forced vital capacity falls below 20 mL/kg or rapid clinical deterioration occurs; physical and occupational therapy during recovery.

Investigational antivirals: Multiple compounds show anti-ZIKV activity in vitro, including sofosbuvir (an NS5B polymerase inhibitor used clinically for hepatitis C), ribavirin, and favipiravir. However, none have demonstrated clinical benefit in human trials. Drug repurposing screens and novel antivirals targeting the NS5 methyltransferase/polymerase domain remain active areas of investigation.

Prevention and Travel Advisories

Personal mosquito protection: The most immediately actionable prevention measure for individuals in or traveling to ZIKV-endemic areas.

Pregnancy travel advisory: The CDC and WHO advise pregnant women to avoid travel to areas with known ZIKV transmission. If travel by a pregnant woman is unavoidable, strict and consistent mosquito avoidance measures are essential throughout the trip. This advisory applies regardless of pregnancy trimester.

Sexual transmission prevention: Given documented sexual transmission and the catastrophic risk to a fetus, the following guidance applies (CDC 2018 guidance):

Blood and organ safety: Blood donation agencies in ZIKV-affected areas implement donor deferral (travelers deferred for 28 days) and nucleic acid testing (NAT) of blood supply. Organ transplantation teams follow specific ZIKV screening protocols.

Vaccine development: Multiple ZIKV vaccine candidates have entered clinical trials, including: a NIAID-developed mRNA-1893 vaccine (Moderna/NIH collaboration) that demonstrated robust immunogenicity in Phase 2 trials; DNA vaccines (Inovio); purified inactivated virus vaccines (Takeda); live-attenuated chimeric vaccines. Complete protection has been demonstrated in animal models. However, the decline in epidemic activity after 2017 created a major obstacle — insufficient incidence in trial sites to demonstrate efficacy endpoints. As of 2024, no ZIKV vaccine is licensed for human use.

Novel vector control strategies:

Prognosis

Acute ZIKV infection in adults: Prognosis is excellent. The vast majority of infections (80%) are asymptomatic; symptomatic disease is mild and self-limiting, typically resolving within 7 days without complications. Fatalities directly attributable to acute ZIKV infection are exceedingly rare in immunocompetent adults. Immunocompromised individuals (transplant recipients, HIV-positive persons with advanced immunosuppression) may experience more severe or prolonged viremia and are at higher risk for complications.

Guillain-Barré syndrome: Most patients recover significant function, though recovery is often prolonged over weeks to months. Approximately 5% of GBS patients have residual disability at 12 months. With optimal ICU and rehabilitation care, mortality is approximately 3–5%; in resource-limited settings, respiratory failure can be fatal. Early initiation of IVIG or plasmapheresis shortens time to recovery.

Congenital Zika Syndrome — highly variable:

Recent Research

Vaccine development: The mRNA platform has shown particular promise for ZIKV vaccines. The NIAID/Moderna mRNA-1893 vaccine demonstrated robust neutralizing antibody responses in Phase 2 human trials. However, the post-2017 collapse of epidemic ZIKV activity in the Americas has created a critical barrier — insufficient disease incidence at trial sites to enroll and power an efficacy trial. Novel trial designs (controlled human infection models, immunological correlates of protection) are being explored to bridge this gap.

Antiviral targets: The ZIKV NS5 protein (which contains both an N-terminal methyltransferase domain capping viral RNA and a C-terminal RNA-dependent RNA polymerase) is the most validated drug target. Sofosbuvir, an FDA-approved hepatitis C NS5B analogue, demonstrates in vitro anti-ZIKV activity. Structure-based drug design targeting the NS5 methyltransferase active site is an active area of medicinal chemistry research. No candidate has advanced to Phase 3 trials for ZIKV as of 2024.

AXL receptor as a therapeutic target: Given AXL's critical role as a ZIKV entry receptor on neural progenitor cells, AXL tyrosine kinase inhibitors (such as bemcentinib/BGB324, already in clinical trials for cancer) have been tested in ZIKV NPC infection models. AXL inhibition reduces ZIKV replication in cortical organoids ("mini-brains") in vitro, though clinical translation remains distant.

Male reproductive tract reservoir: The mechanisms by which ZIKV persists in Sertoli cells and evades testicular immune surveillance are under active investigation. Understanding viral clearance from the male genital tract is critical for refining sexual transmission prevention guidance and for potential antiviral targeting of the semen reservoir.

CZS neurodevelopmental longitudinal cohorts: Long-term follow-up studies of Brazilian CZS cohorts — particularly the MERG (Microcephaly Epidemic Research Group) in Pernambuco — are documenting the full developmental trajectory of affected children, including "slow CZS" presentations, epilepsy burden, and social integration outcomes. These data are essential for healthcare planning and for understanding the full spectrum of ZIKV teratogenicity.

Wolbachia and vector control at scale: The World Mosquito Program's city-scale Wolbachia release in Yogyakarta, Indonesia — a 2020 New England Journal of Medicine randomized controlled trial — demonstrated a 77% reduction in dengue incidence and 86% reduction in dengue hospitalizations. Since ZIKV and dengue share the same Aedes aegypti vector, these results are highly relevant for ZIKV control. Expansion of Wolbachia programs is ongoing across Latin America, Southeast Asia, and the Pacific.

Improved ZIKV-specific diagnostics: Development of ZIKV-specific serological assays that can distinguish ZIKV immunity from dengue and yellow fever vaccine responses remains an active research priority. Epitope-specific antibody assays and NS1-based antigens that exploit structural differences between flavivirus NS1 proteins show promise for improved specificity.

References

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Research Papers

The following PubMed topic searches retrieve current peer-reviewed literature on Zika Virus.

  1. Zika virus pathogenesis review
  2. Zika virus microcephaly congenital
  3. Zika virus Guillain-Barré syndrome
  4. Zika virus sexual transmission semen
  5. Zika virus pregnancy fetal outcome
  6. Zika virus neural progenitor cells AXL
  7. Zika virus vaccine clinical trial
  8. Aedes aegypti Zika arbovirus control
  9. Zika virus diagnosis RT-PCR serology
  10. Congenital Zika syndrome neurodevelopment
  11. Zika virus 2016 PHEIC WHO outbreak
  12. Zika virus antiviral treatment sofosbuvir

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