FOCUS ON … The ZIKA virus

Epidemiology

Zika virus is a single stranded RNA of the genus Flavivirus. This is a closely related arbovirus of the dengue, yellow fever, West Nile viruses and Japanese encephalitis, and is transmitted by mosquitoes of the Aedes genus. Especially Aedes albopictus and Aedes aegypti. This virus is named after the Zika forest in Uganda where it was first discovered in a rhesus monkey in 1947. The virus was later isolated in humans with fever in West Africa. After spreading worldwide, it is now regularly encountered in Africa and Asia.

There are two Zika virus lineages, an Africa lineage and an Asian lineage, responsible for epidemics in many countries: Indonesia, Micronesia, Thailand, Philippines. In 2013, the French Polynesia was affected by an epidemic due to the Asian lineage of Zika, with an estimated 32,000 cases and the epidemic spread to New Caledonia in 2014. In May 2015, the epidemic hit Brazil, affecting between 440,000 and 1.3 million persons. This was the first time that Zika virus was found in South America, and a possible explanation of its presence in Brazil could be the introduction of the virus during the World Cup in 2014. In January 2016, 16 neighbouring countries in South America reported indigenous cases of Zika, including the French Antilles (Martinique, Guadeloupe, St. Maarten) and French Guiana.

To date, no indigenous cases have been reported in Europe, only a few imported cases in various countries.

Transmission

The most common method of transmission vectoral via through bites of female Aedes mosquito. The mosquito becomes infected by biting an infected human, and after incubation in the mosquito of 3 to 10 days, the virus reaches the insect’s salivary glands from where it can be transmitted by the host biting a healthy human.

Transmission through blood transfusion is also possible if the blood is taken when the donor is in the viremic phase.

Sexual contamination is possible, based on patients who have not travelled, and who were contaminated outside the period of activity of the mosquito vector by a partner who did travel in epidemic areas. The virus has also been detected in semen by PCR [3].

Maternal-fetal transmission may occur in all trimesters of pregnancy. However, the risk of transmission with brain abnormality of the microcephaly type is at a maximum in the first trimester of pregnancy. The association with central neurological complications in the fetus is primarily statistical with a sharp increase in the number of microcephalies in epidemic areas. Zika virus has already been detected by PCR in amniotic fluid but as yet no evaluation of cerebrospinal fluid of neonates with abnormalities of the central nervous system is available. The virus has however been detected in samples from a neonate suffering from microcephaly and hydrops, who died in the first 5 minutes of life.

Clinical symptomatology

In previous epidemics (French Polynesia in 2013, New Caledonia in 2014, Brazil in 2015), the number of asymptomatic expressions of Zika infection was estimated at between 70 and 80%.

The incubation period is 3 to 12 days. For asymptomatic forms, the identification of a case of suspected Zika includes a pruritic maculopapular rash, with or without fever, accompanied by at least 2 of the following signs: conjunctival hyperemia or conjunctivitis, arthralgia and myalgia, with no other etiology found.

Other signs are less frequently reported: flu-like symptoms with high fever, pain behind the eyes, headache, asthenia. The average duration of the symptoms is 2 to 7 days. The clinical course is spontaneously favourable over twelve days or so, but in a number of cases, neurological complications of the Guillain-Barré syndrome, polyradiculoneuritis type may arise between day 3 and day 23 after the onset of clinical signs. No causal link has yet been formally established, and this is more a question of resurgence of cases of Guillain-Barré syndrome in the period and area of the Zika epidemic. Other neurological complications have been considered such as encephalitis, optic neuritis. There is no direct mortality due to Zika.

Biological diagnosis

Viremia is transient and the viral load is low and of short duration: it begins 2 to 3 days before clinical signs and continues for 3 to 5 days after onset of clinical signs. The presence of the virus is detectable in the early clinical signs in the urine and is more prolonged, up to 10 or even 15 days after the onset of clinical signs. The virus has also been detected in saliva but there is currently no information on the duration and extent of viral load in this matrix. Antibodies only appear later, IgM’s appear from D5 to D7 and IgG’s from D10 to D15, but serology is recommended after 15 days, or even from D30 to D40. When there are no symptoms, indications of biological tests should be assessed on a case by case basis; in cases, PCR tests of the urine can be performed within 10 days of returning from travel in an epidemic zone.

To date no official recommendations have been issued, however, based on current data, it the following points emerge: Given the prevalence of dengue and chikungunya in the French Antilles-Guiana, all suspected cases must undergo diagnostic test for not only Zika, but also dengue and chikungunya according to the following scheme:  

However, due to the short duration of the viremia, negative PCR does not invalidate a diagnosis of Zika. Treatment is symptomatic and to date no vaccine is available. Protection against mosquitoes is the key in the fight against Zika:

• Collective protection: fight against breeding sites, i.e. removal of standing water in the home and beyond.
• Personal protection against bites by wearing long and light clothing, use of repellents (impregnated mosquito nets at night, impregnation of clothes, repellents on exposed areas). It is a primary importance to improve the protection of pregnant women and Zika sufferers.

References

• A diagnostic polymerase chain reaction assay for Zika virus.
  Balm MN, Lee CK, Lee HK, Chiu L, Koay ES, Tang JW.
  J Med Virol. 2012 Sep;84(9):1501-5. doi: 10.1002/jmv.23241.
• Zika fever imported from Thailand to Japan, and diagnosed by PCR in the urines.
  Shinohara K, Kutsuna S, Takasaki T, Moi ML, Ikeda M, Kotaki A, Yamamoto K, Fujiya Y, Mawatari M, Takeshita N, Hayakawa K, Kanagawa S, Kato Y, Ohmagari N.
  J Travel Med. 2016 Jan 18;23(1). pii: tav011. doi: 10.1093/jtm/tav011. Print 2016 Jan.
• Rapid communications POTENTIAL FOR ZIKA VIRUS TRANSMISSION THROUGH BLOOD TRANSFUSION DEMONSTRATED DURING AN OUTBREAK IN FRENCH POLYNESIA, NOVEMBER 2013 TO FEBRUARY 2014
  Eurosurveillance, Volume 19, Issue 14, 10 April 2014 –
•  EUROPEAN CENTER FOR DISEASE PREVENTION AND CONTROLE “ZIKA VIRUS EPIDEMIC IN THE AMERICAS: POTENTIAL ASSOCIATION WITH MICROCEPHALY AND GUILLAIN-BARRÉ SYNDROME” STOCKHOLM 2015
• Rapid spread of Zika virus in the Americas
  Petersen et al.
  International Journal of Infectious Diseases, volume 44 (11-15), 2016