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Zika Virus: the Latest Newcomer.

Saiz JC, Vázquez-Calvo Á, Blázquez AB, Merino-Ramos T, Escribano-Romero E, Martín-Acebes MA - Front Microbiol (2016)

Bottom Line: Zika virus (ZIKV), a flavivirus transmitted by Aedes mosquitoes, was identified in 1947 in a sentinel monkey in Uganda, and later on in humans in Nigeria.ZIKV infection was characterized by causing a mild disease presented with fever, headache, rash, arthralgia, and conjunctivitis, with exceptional reports of an association with Guillain-Barre syndrome (GBS) and microcephaly.Clarifying such worrisome relationships is, thus, a current unavoidable goal.

View Article: PubMed Central - PubMed

Affiliation: Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria Madrid, Spain.

ABSTRACT
Since the beginning of this century, humanity has been facing a new emerging, or re-emerging, virus threat almost every year: West Nile, Influenza A, avian flu, dengue, Chikungunya, SARS, MERS, Ebola, and now Zika, the latest newcomer. Zika virus (ZIKV), a flavivirus transmitted by Aedes mosquitoes, was identified in 1947 in a sentinel monkey in Uganda, and later on in humans in Nigeria. The virus was mainly confined to the African continent until it was detected in south-east Asia the 1980's, then in the Micronesia in 2007 and, more recently in the Americas in 2014, where it has displayed an explosive spread, as advised by the World Health Organization, which resulted in the infection of hundreds of thousands of people. ZIKV infection was characterized by causing a mild disease presented with fever, headache, rash, arthralgia, and conjunctivitis, with exceptional reports of an association with Guillain-Barre syndrome (GBS) and microcephaly. However, since the end of 2015, an increase in the number of GBS associated cases and an astonishing number of microcephaly in fetus and new-borns in Brazil have been related to ZIKV infection, raising serious worldwide public health concerns. Clarifying such worrisome relationships is, thus, a current unavoidable goal. Here, we extensively review what is currently known about ZIKV, from molecular biology, transmission routes, ecology, and epidemiology, to clinical manifestations, pathogenesis, diagnosis, prophylaxis, and public health.

No MeSH data available.


Related in: MedlinePlus

Schematic view of the ZIKV cellular lifecycle. See text for details.
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Figure 2: Schematic view of the ZIKV cellular lifecycle. See text for details.

Mentions: It has been described that ZIKV enters the cell using adhesion factors such as DC-SIGN (Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin) and diverse members of the phosphatidylserine receptor family (Hamel et al., 2015). Once the attached viral particles are internalized into the cell (Figure 2), the viral genome should be released inside the cytoplasm to start translation and replication. The mechanism of penetration of the flavivirus genome into the cytoplasm is initiated by the fusion of the viral envelope with the membranes of the cellular endosomes from the host cell, a process triggered by acidic pH inside cellular endosomes (Stiasny et al., 2011; Vazquez-Calvo et al., 2012). This mechanism of penetration is consistent with, as mentioned before, an early observation showing that ZIKV particles were sensible to acidic pH, and were inactivated by treatment with acidic pH lower than 6.2 (Dick, 1952). Along this line, the sensitivity of ZIKV particles to acidic pH is consistent with the observation performed with other flaviviruses indicating that, in the absence of target membranes, the exposure of flavivirus virions to acidic pH induces rearrangements of the E glycoprotein, which result in a loss of infectivity (Gollins and Porterfield, 1986). The viral RNA acts as mRNA inside the cytoplasm of the infected cell, and negative-strand viral RNA is synthesized and directs positive-strand RNA synthesis in association with a virus-induced network of membranes derived from the endoplasmic reticulum, ER (Figure 2). Electron microscopy studies of virus infected cells showed that ZIKV virions are found in short chains within tubular elements of the ER, which appeared to be in continuity with distended cisternae (Bell et al., 1971). These images were similar to membrane rearrangements observed in other flavivirus infected cells (Welsch et al., 2009; Martin-Acebes et al., 2011; Miorin et al., 2013). Although flavivirus replication is thought to occur in the cellular cytoplasm, it should be noted that one study reported that ZIKV antigens could be found in infected cell nuclei (Buckley and Gould, 1988).


Zika Virus: the Latest Newcomer.

Saiz JC, Vázquez-Calvo Á, Blázquez AB, Merino-Ramos T, Escribano-Romero E, Martín-Acebes MA - Front Microbiol (2016)

Schematic view of the ZIKV cellular lifecycle. See text for details.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4835484&req=5

Figure 2: Schematic view of the ZIKV cellular lifecycle. See text for details.
Mentions: It has been described that ZIKV enters the cell using adhesion factors such as DC-SIGN (Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin) and diverse members of the phosphatidylserine receptor family (Hamel et al., 2015). Once the attached viral particles are internalized into the cell (Figure 2), the viral genome should be released inside the cytoplasm to start translation and replication. The mechanism of penetration of the flavivirus genome into the cytoplasm is initiated by the fusion of the viral envelope with the membranes of the cellular endosomes from the host cell, a process triggered by acidic pH inside cellular endosomes (Stiasny et al., 2011; Vazquez-Calvo et al., 2012). This mechanism of penetration is consistent with, as mentioned before, an early observation showing that ZIKV particles were sensible to acidic pH, and were inactivated by treatment with acidic pH lower than 6.2 (Dick, 1952). Along this line, the sensitivity of ZIKV particles to acidic pH is consistent with the observation performed with other flaviviruses indicating that, in the absence of target membranes, the exposure of flavivirus virions to acidic pH induces rearrangements of the E glycoprotein, which result in a loss of infectivity (Gollins and Porterfield, 1986). The viral RNA acts as mRNA inside the cytoplasm of the infected cell, and negative-strand viral RNA is synthesized and directs positive-strand RNA synthesis in association with a virus-induced network of membranes derived from the endoplasmic reticulum, ER (Figure 2). Electron microscopy studies of virus infected cells showed that ZIKV virions are found in short chains within tubular elements of the ER, which appeared to be in continuity with distended cisternae (Bell et al., 1971). These images were similar to membrane rearrangements observed in other flavivirus infected cells (Welsch et al., 2009; Martin-Acebes et al., 2011; Miorin et al., 2013). Although flavivirus replication is thought to occur in the cellular cytoplasm, it should be noted that one study reported that ZIKV antigens could be found in infected cell nuclei (Buckley and Gould, 1988).

Bottom Line: Zika virus (ZIKV), a flavivirus transmitted by Aedes mosquitoes, was identified in 1947 in a sentinel monkey in Uganda, and later on in humans in Nigeria.ZIKV infection was characterized by causing a mild disease presented with fever, headache, rash, arthralgia, and conjunctivitis, with exceptional reports of an association with Guillain-Barre syndrome (GBS) and microcephaly.Clarifying such worrisome relationships is, thus, a current unavoidable goal.

View Article: PubMed Central - PubMed

Affiliation: Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria Madrid, Spain.

ABSTRACT
Since the beginning of this century, humanity has been facing a new emerging, or re-emerging, virus threat almost every year: West Nile, Influenza A, avian flu, dengue, Chikungunya, SARS, MERS, Ebola, and now Zika, the latest newcomer. Zika virus (ZIKV), a flavivirus transmitted by Aedes mosquitoes, was identified in 1947 in a sentinel monkey in Uganda, and later on in humans in Nigeria. The virus was mainly confined to the African continent until it was detected in south-east Asia the 1980's, then in the Micronesia in 2007 and, more recently in the Americas in 2014, where it has displayed an explosive spread, as advised by the World Health Organization, which resulted in the infection of hundreds of thousands of people. ZIKV infection was characterized by causing a mild disease presented with fever, headache, rash, arthralgia, and conjunctivitis, with exceptional reports of an association with Guillain-Barre syndrome (GBS) and microcephaly. However, since the end of 2015, an increase in the number of GBS associated cases and an astonishing number of microcephaly in fetus and new-borns in Brazil have been related to ZIKV infection, raising serious worldwide public health concerns. Clarifying such worrisome relationships is, thus, a current unavoidable goal. Here, we extensively review what is currently known about ZIKV, from molecular biology, transmission routes, ecology, and epidemiology, to clinical manifestations, pathogenesis, diagnosis, prophylaxis, and public health.

No MeSH data available.


Related in: MedlinePlus