Zika virus

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Zika virus
Zika EM CDC 280116.tiff

Electron microscope image of Zika virus particles
(darkly contrasted, about 40  nm in diameter) in cells of a cell culture

Systematics
Classification : Viruses
Area : Riboviria
Empire : Orthornavirae
Phylum : Kitrinoviricota
Class : Flasuviricetes
Order : Amarillovirales
Family : Flaviviridae
Genre : Flavivirus
Type : Zika virus
Taxonomic characteristics
Genome : (+) ssRNA linear
Baltimore : Group 4
Symmetry : icosahedral
Cover : available
Scientific name
Zika virus
Short name
ZIKV
Left
NCBI  Taxonomy: 64320
NCBI  Reference: NC_012532
ICTV Taxon History: 201853123
ICTVdB Virus Code : 00.026.0.01.055

The Zika virus ( listen ? / I ) ( ZIKV ) belongs to the genus Flavivirus of the family Flaviviridae . It was first isolated in 1947 from a rhesus monkey (a so-called marker animal or sentinel monkey ) held captive to find the yellow fever virus at a research station in the Zika Forest in Entebbe , Uganda , and named after the location. The virus is endemic to Africa and Southeast Asia , the different strains of the virus are therefore divided into an African and an Asian group. Since infections with the Zika virus (" Zika fever ") and newly observed damage to fetuses in pregnant women have been observed in Latin America for the first time since 2015 , the World Health Organization (WHO) declared on February 1, 2016 a "public health emergency of international proportions". Audio file / audio sample

construction

Genome

The basic structure and the possible virus proteins of the Zika virus do not differ significantly from other representatives of the genus Flavivirus . The Zika virus is most closely related to the (not yet officially confirmed) ' Spondweni virus ', with which it forms a clade within the mosquito-borne flaviviruses. The virus genome consists of a 10,794  base long single- stranded RNA of positive polarity , which contains an approximately 10,300 base long open reading frame which codes for the virus proteins and is flanked at the 5 ' and 3' ends by non-coding sequences . The 5 'end has a cap structure and the 3' end does not have a poly-A tail , but forms a loop-shaped secondary structure . This loop is recognized by the cellular RNase XRN1 and cleaved from the genome. The released 3 'end ( subgenomic flavivirus RNA , sfRNA) is involved as a virulence factor in the pathogenicity of the flaviviruses, presumably through the inhibition of the cellular resistance factor RIG-I . The first complete sequence of the virus genome of an isolate was published in 2006. In the course of protein biosynthesis, a polyprotein of around 3417 to 3423  amino acids is formed from the RNA genome , which is then split into the individual viral proteins by viral and cellular proteases .

Close relatives of the Zika virus are the flaviviruses dengue virus and West Nile virus , which are also transmitted by Aedes mosquitoes and have been classified as emerging pathogens , but can cause far more severe diseases in humans.

Virus proteins

After complete sequencing of the virus genome of an isolate from French Polynesia from 2013, the following possible virus proteins were derived from the nucleotide sequence:

Virion

Zika virus virions (stained red) on a sheathed nerve cell ( TEM image )

The virion has a diameter of around 50 nanometers and an icosahedral shape of the virus envelope and capsid, with three homodimers of the E protein ( receptor , transmembrane protein and fusogenic protein ) on each surface on the outside. The E protein has serine protease activity. The other transmembrane protein M is partially covered by the E protein in the virus envelope. The capsid made of the capsid protein C, which encases the viral RNA, lies under the virus envelope.

Replication cycle

3-D reconstruction of the Zika virus

After the viral receptor E-protein has bound to a previously unknown cellular surface protein, the virion is invaginated into an endosome by endocytosis . In the endosome, the E protein, as a fusogenic protein, ensures the fusion of the virus envelope and the endosome membrane, which releases the capsid into the cytosol . There the capsid and the RNA genome are unpacked. The genome is replicated in the cytosol by the RNA polymerase NS5, in which double-stranded viral RNA is formed. Since the RNA genome has a positive polarity, the viral polyprotein is generated directly (without replication) from the copied RNA genomes and at the same time from the unpacked RNA strand by protein synthesis, which is then split into the individual viral proteins by proteolysis. The assembly of a newly formed virion takes place in the endoplasmic reticulum . After a transfer into the Golgi apparatus , the virion matures by proteolysis of the protein prM . Zika viruses are non-lytic viruses and leave the host cell by exocytosis .

The tropism of the Zika virus includes, among other things, cells of the skin and neural stem cells . Because of the infection of neuronal embryonic stem cells, the damage probably occurs during the neuronal development of embryos. The Zika virus leads to neuronal infections in mouse fetuses and, as a result, to neuronal defects.

Infection in humans

The Zika virus causes Zika fever in humans.

Epidemiology

Countries in which Zika virus infections through mosquito transmission have occurred in the past (as of January 2016). confirmed infections acquired in the region Infections so far only proven serologically



The Zika virus was first detected in humans in 1952 in Uganda and Tanzania . In the following decades the virus spread widely in Africa and Asia. However, as of 2007, fewer than 15 human infections were known, all of which were found in Africa or Southeast Asia.

The first major outbreak in humans - on the Yap Islands in Micronesia in 2007 - led to the Zika virus being classified as an emergent virus , i.e. a pathogen that could possibly spread even further across the world. This was followed by an epidemic in French Polynesia in 2013-2014 , in which an increased incidence of Guillain-Barré syndrome (GBS) was observed for the first time , as well as transmission to the unborn child.

From 2015 onwards, increasing numbers of Zika fever cases were observed in South, Central America and the Caribbean, all of which were caused by the Asian line of the Zika virus. Phylogenetically , it is believed that the virus arrived in America as early as 2013. From 2015 outbreaks back in Africa ( Cape Verde , Guinea-Bissau and Angola ) were described, which were also triggered by the Asian line.

The 2015 Latin American outbreak is described as a “perfect storm” because a new line, the American subclade, hit a completely susceptible population and infected 60% of the exposed population.

The first endemic Zika virus transmissions by mosquitoes in Europe were reported from southern France in autumn 2019.

transmission

The natural occurrence of the Zika virus is in tropical Africa; However, there are cases of infection in the entire tropical climate zone. Occasionally, travelers have carried the virus to other climate zones, such as Europe.

The biology and transmission routes of the Zika virus had been little researched until the end of 2015. It was known, however, that the viruses are mainly transmitted by mosquitoes of the Aedes aegypti species and other species of the Aedes genus , possibly including the Asian tiger mosquito ( Aedes albopictus ). In several laboratory experiments since 2016 it has been shown that Aedes albopictus can also transmit the viruses - but only at temperatures above 27 degrees. Whether and to what extent mosquitoes of the Culex species transmit the Zika virus is currently being investigated (2019). The vector competence of Cx is best researched. quinquefasciatus. ZIKV-RNA has never been detected in mosquitoes of this type in a field study. The ability to transmit in the laboratory has been refuted by a large number of studies. There are also experimental results to support this. The fact that endemic Culex species are involved in the transmission of Zika viruses in Central Europe can currently be ruled out with great certainty. Most comprehensive was the lack of a relevant experimental vector competence for Zika for the three most common species in Central Europe Cx. p. pipiens, Cx. p. molestus and Cx. torrentium.

Transmission through sexual contact between people is also possible, although so far only isolated cases are known. A case was documented as early as 2009 in which a biologist from Colorado State University is said to have infected his wife with the virus. In early February 2016, there were renewed reports that human sexual transmission was detected in Dallas . In October 2016, a journal published that the complete virus genome had been isolated from seminal fluid . According to a study published in 2019, the viruses were still detectable in sperm samples in 8 of 97 patients with initially high viral loads up to 38 days after the initial diagnosis.

Zika virus genetic material has also been detected in the urine and saliva of symptomatic patients . It is not yet known to what extent the Zika viruses can also be transmitted through urine and saliva.

Course of infection

Zika virus manifestation rash in Brazil

The infection processes that have become known were initially relatively mild, and only one in five infected people developed symptoms: in particular rash and fever ("Zika fever"), joint pain, conjunctivitis and, less often, muscle pain, headache and vomiting. The symptoms usually subside after a few days, at the latest after a week. So far there are no confirmed deaths. However, there are suspected cases in Colombia in which three patients developed Guillain-Barré syndrome after a Zika infection and this would have led to the death of the sick. In a study with patients from French Polynesia , an accumulation of Guillain-Barré syndromes was found with serological evidence of previous or recent infection with the Zika virus. In the examined serum samples from 42 patients with Guillain-Barré syndrome, specific antibodies against the Zika virus could be detected, in some patients additional antibodies against other tropical arboviruses . None of these patients with GBS died from it.

Infections in pregnancy

Schematic representation of microcephaly

Based on the epidemiological data, there has been an urgent suspicion of a connection between infections with the Zika virus in pregnant women during the first trimester of pregnancy and microcephaly in fetuses and newborns since the end of 2015 .

At the beginning of 2016, the first reliable virological evidence of an infection of the fetal brain with the Zika virus in existing microcephaly was provided:

A woman who was in Natal (Brazil) became pregnant there and fell ill in the 13th  week of pregnancy with all clinical signs of Zika fever. The ultrasound examination showed no morphological abnormalities in the fetus in the 14th and 20th week of pregnancy. Back in Ljubljana , the first signs of microcephaly were found in the fetus in the 29th week of pregnancy, followed by severe microcephaly (brain size below the 2nd percentile), intracerebral calcifications , an enlargement of the cerebral ventricles and a severe general growth disorder (weight of the Fetus below the 3rd percentile). Calcifications were also found in the placenta . After the termination of pregnancy, viral RNA of the Zika virus was found in the brain tissue of the fetus. Its entire genome has been sequenced. The virus isolate was 99.7 percent identical at the RNA level to an isolate from French Polynesia that was sequenced in 2013. No Zika virus was detected in other organs (placenta, heart, lungs, skin, thymus, spleen, liver, and kidneys) . An electron microscopic examination of the brain tissue revealed flavivirus-like particles.

The damage to the fetal brain begins from the 20th week of pregnancy with a disruption of the maturation of the cortex and the delay in gyral folding. It is also unusual that the virus persisted in the fetus for 21 weeks and that the IgG antibodies formed after the maternal infection were not able to terminate the infection in the fetus after the acute infection had healed.

The results support the previous detection of Zika virus RNA in the amniotic fluid in two microcephalic fetuses in Brazil in the 29th and 30th week of gestation respectively. In these two cases, too, the viral RNA corresponded to the Asian Zika virus isolates. In April 2016, after evaluating various studies, the US health authority CDC came to the conclusion that the Zika virus clearly causes the malformation of the skull, microcephaly in fetuses. In December 2016, a first, larger study on pregnant women found evidence that a Zika virus infection significantly increased the risk of malformations and other damage compared to a control group.

According to current knowledge, Zika fever is not more severe, longer or with a higher frequency of complications for pregnant women than for non-pregnant women.

Previous dengue infections protect against Zika-associated damage to the fetus.

diagnosis

Diagnosing Zika virus infections based on clinical symptoms is difficult as there are other endemic arboviruses in the corresponding regions that produce very similar nonspecific clinical symptoms. The Zika virus could be detected by RT-PCR in acutely ill patients . The viremic phase , in which this detection from the blood is successful, can, however, be short with only a few days. For this reason, the World Health Organization recommends performing RT-PCR tests on serum samples within one to three days of the onset of symptoms, and additionally within three to five days of the onset of symptoms in saliva or urine samples. Serological tests for the detection of specific IgM and IgG antibodies have also been used, although their informative value with regard to specificity and sensitivity is limited. IgM can usually be detected within three days of the onset of the disease. The antibody detection, especially the IgM detection, can produce false positive results, since serological cross-reactivity with closely related (i.e. from the same genus) flaviviruses such as dengue virus and West Nile virus or after vaccinations against flaviviruses ( yellow fever virus , TBE virus) Virus ) are possible.

The Centers for Disease Control and Prevention (CDC) in the USA point out that the differential diagnosis of Zika infections, based on the typical clinical signs, is very broad and that a large number of other viral and bacterial infections must be differentiated. In Latin America in particular, the common dengue virus must be ruled out, as it can cause similar general symptoms and a similar rash in acute infection. The viral causes are infections with rubella virus , measles virus and parvovirus B19 (all with a possible exanthema) as well as non-exanthematic infections with enteroviruses , adenoviruses and various alphaviruses (e.g. Chikungunya virus , Mayaro virus , Ross River) virus , Barmah Forest virus , O'nyong-nyong virus and Sindbis virus ) the differential diagnosis. Leptospirosis , rickettsiosis and A-streptococcal infections are to be distinguished as bacterial infectious diseases , which, however, similar to malaria , which can always be ruled out in the tropics, also have characteristic symptoms.

According to information from the Society for Virology from April 2016, a new ZIKV NS1 antigen-based test now enables a clear diagnosis of a previous Zika virus infection after a few hours. Researchers were able to prove that this new test for the detection of ZIKV antibodies is also highly specific if the person to be examined has an earlier and laboratory-proven TBE infection or vaccination.

protection

So far, there is no vaccination or disease prevention medication . Many scientists believe that it could be years before a vaccine is available. The first potential vaccines have been tested in Phase I studies since July 2016 , but the first results will not be available before the end of 2017. The only protective measures that apply are therefore general protection against mosquito bites or even avoidance of corresponding climatic zones. Based on reports of sexual transmission of the virus, general protective measures against sexually transmitted diseases, such as the use of condoms in particular, apply .

It is not yet known whether an infection, once passed, leads to at least temporary immunity.

Reporting requirement

In Germany, the direct or indirect detection of the Zika virus must be reported by name in accordance with Section 7 of the Infection Protection Act (IfSG), provided the evidence indicates an acute infection. Laboratories etc. are required to report ( Section 8 IfSG).

In Austria, Zika virus infections are notifiable diseases in accordance with Section 1 (1) No. 2 of the 1950 Epidemic Act . Cases of illness and death must be reported. Doctors and laboratories, among others, are obliged to report this ( Section 3 Epidemics Act).

In Switzerland, positive laboratory results for the Zika virus must be reported by the testing laboratory in accordance with the Epidemics Act (EpG) in conjunction with the Epidemics Ordinance and Appendix 3 of the EDI Ordinance on the reporting of observations of communicable diseases in humans . In addition, Zika fever is a reportable disease according to the standards mentioned and Appendix 1 of the EDI ordinance mentioned.

Web links

Commons : Zika virus  - collection of pictures, videos and audio files

Individual evidence

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