scholarly journals Potential for Zika virus to establish a sylvatic transmission cycle in the Americas

2016 ◽  
Author(s):  
Benjamin M. Althouse ◽  
Nikos Vasilakis ◽  
Amadou A. Sall ◽  
Mawlouth Diallo ◽  
Scott C. Weaver ◽  
...  
Keyword(s):  
Zika Virus ◽  
New World ◽  
Vector Competence ◽  
Host Population ◽  
Transmission Model ◽  
New World Monkeys ◽  
Sylvatic Cycle ◽  
Transmission Cycle ◽  
Force Of Infection ◽  
Congenital Zika Syndrome

AbstractZika virus (ZIKV) originated and continues to circulate in a sylvatic transmission cycle between non-human primate hosts and arboreal mosquitoes in tropical Africa. Recently ZIKV invaded the Americas, where it poses a threat to human health, especially to pregnant women and their infants. Here we examine the risk that ZIKV will establish a sylvatic cycle in the Americas, focusing on Brazil. We review the natural history of sylvatic ZIKV and present a mathematical dynamic transmission model to assess the probability of establishment of a sylvatic ZIKV transmission cycle in non-human primates and/or other mammals and arboreal mosquito vectors in Brazil. Brazil is home to multiple species of primates and mosquitoes potentially capable of ZIKV transmission, though direct assessment of host competence (ability to mount viremia sufficient to infect a feeding mosquito) and vector competence (ability to become infected with ZIKV and disseminate and transmit upon subsequent feedings) of New World species is lacking. Modeling reveals a high probability of establishment of sylvatic ZIKV across a large range of biologically plausible parameters. Probability of establishment is dependent on host population sizes and birthrates and ZIKV force of infection, but a network of as few as 6,000 primates with 10,000 mosquitoes is capable of supporting establishment of a ZIKV sylvatic cycle. Research on the susceptibility of New World monkeys or other small mammals to ZIKV, on the vector competence of New World Aedes, Sabethes, and Haemagogus mosquitoes for ZIKV, and on the geographic range of these species is urgently needed. A sylvatic cycle of ZIKV would make future elimination efforts in the Americas practically impossible, and paints a dire situation for the epidemiology of ZIKV and ending the ongoing outbreak of congenital Zika syndrome.

scholarly journals Colonized Sabethes cyaneus, a Sylvatic New World Mosquito Species, Shows a Low Vector Competence for Zika Virus Relative to Aedes aegypti

Viruses ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 434 ◽  
Author(s):  
Ajit K. Karna ◽  
Sasha R. Azar ◽  
Jessica A. Plante ◽  
Rumei Yun ◽  
Nikos Vasilakis ◽  
...  
Keyword(s):  
Aedes Aegypti ◽  
Yellow Fever ◽  
Zika Virus ◽  
New World ◽  
Yellow Fever Virus ◽  
Vector Competence ◽  
Mosquito Species ◽  
Sylvatic Cycle ◽  
Post Feeding ◽  
Body Compartments

The introduction of Zika virus (ZIKV) to the Americas raised concern that the virus would spill back from human transmission, perpetuated by Aedes aegypti, into a sylvatic cycle maintained in wildlife and forest-living mosquitoes. In the Americas, Sabethes species are vectors of sylvatic yellow fever virus (YFV) and are therefore candidate vectors of a sylvatic ZIKV cycle. To test the potential of Sabethes cyaneus to transmit ZIKV, Sa. cyaneus and Ae. aegypti were fed on A129 mice one or two days post-infection (dpi) with a ZIKV isolate from Mexico. Sa. cyaneus were sampled at 3, 4, 5, 7, 14, and 21 days post-feeding (dpf) and Ae. aegypti were sampled at 14 and 21 dpf. ZIKV was quantified in mosquito bodies, legs, and saliva to measure infection, dissemination, and potential transmission, respectively. Of 69 Sa. cyaneus that fed, ZIKV was detected in only one, in all body compartments, at 21 dpf. In contrast, at 14 dpf 100% of 20 Ae. aegypti that fed on mice at 2 dpi were infected and 70% had virus in saliva. These data demonstrate that Sa. cyaneus is a competent vector for ZIKV, albeit much less competent than Ae. aegypti.

scholarly journals Zika viruses of both African and Asian lineages cause fetal harm in a vertical transmission model

2018 ◽  
Author(s):  
Anna S. Jaeger ◽  
Reyes A. Murreita ◽  
Lea R. Goren ◽  
Chelsea M. Crooks ◽  
Ryan V. Moriarty ◽  
...  
Keyword(s):  
Mouse Model ◽  
Vertical Transmission ◽  
Birth Defects ◽  
Asian American ◽  
Zika Virus ◽  
French Polynesia ◽  
Transmission Model ◽  
Foreseeable Future ◽  
Zikv Infection ◽  
Congenital Zika Syndrome

AbstractCongenital Zika virus (ZIKV) infection was first linked to birth defects during the American outbreak 1–3. It has been proposed that mutations unique to the Asian/American-genotype explain, at least in part, the ability of Asian/American ZIKV to cause congenital Zika syndrome (CZS) 4,5. Recent studies identified mutations in ZIKV infecting humans that arose coincident with the outbreak in French Polynesia and were stably maintained during subsequent spread to the Americas 5. Here we show that African ZIKV can infect and harm fetuses and that the S139N mutation that has been associated with the American outbreak is not essential for fetal harm. Our findings, in a vertical transmission mouse model, suggest that ZIKV will remain a threat to pregnant women for the foreseeable future, including in Africa, southeast Asia, and the Americas. Additional research is needed to better understand the risks associated with ZIKV infection during pregnancy, both in areas where the virus is newly endemic and where it has been circulating for decades.

scholarly journals High susceptibility, viral dynamics and persistence of South American Zika virus in New World monkeys

2019 ◽  
Vol 1 (1A) ◽  
Author(s):  
Neil Berry ◽  
Claire Ham ◽  
Jo Hall ◽  
Adrian Jenkins ◽  
Elaine Giles ◽  
...  
Keyword(s):  
Zika Virus ◽  
New World ◽  
New World Monkeys ◽  
South American ◽  
Viral Dynamics ◽  
High Susceptibility

scholarly journals Two sides of a coin: a Zika virus mutation selected in pregnant rhesus macaques promotes fetal infection in mice but at a cost of reduced fitness in nonpregnant macaques and diminished transmissibility by vectors

2020 ◽  
Author(s):  
Danilo Lemos ◽  
Jackson B. Stuart ◽  
William Louie ◽  
Anil Singapuri ◽  
Ana L. Ramírez ◽  
...  
Keyword(s):  
Zika Virus ◽  
Fetal Death ◽  
Rhesus Macaques ◽  
Low Frequency ◽  
Alternate Host ◽  
Transmission Cycle ◽  
Fetal Infection ◽  
Congenital Zika Syndrome ◽  
Pregnant Mice ◽  
Mouse Fetuses

ABSTRACTAlthough fetal death is now understood to be a severe outcome of congenital Zika syndrome, the role of viral genetics is still unclear. We sequenced Zika virus (ZIKV) from a rhesus macaque fetus that died after inoculation and identified a single intra-host mutation, M1404I, in the ZIKV polyprotein, located in NS2B. Targeted sequencing flanking position 1404 in 9 additional macaque mothers and their fetuses identified M1404I at sub-consensus frequency in the majority (5 of 9, 56%) of animals and some of their fetuses. Despite its repeated presence in pregnant macaques, M1404I occurs rarely in humans since 2015. Since the primary ZIKV transmission cycle is human-mosquito-human, mutations in one host must be retained in the alternate host to be perpetuated. We hypothesized that ZIKV I1404 increases fitness in non-pregnant macaques and pregnant mice but is less efficiently transmitted by vectors, explaining its low frequency in humans during outbreaks. By examining competitive fitness relative to M1404, we observed that I1404 produced lower viremias in non-pregnant macaques and was a weaker competitor in tissues. In pregnant wildtype mice ZIKV I1404 increased the magnitude and rate of placental infection and conferred fetal infection, contrasting with M1404, which was not detected in fetuses. Although infection and dissemination rates were not different, Ae. aegypti transmitted ZIKV I1404 more poorly than M1404. Our data highlight the complexity of arbovirus mutation-fitness dynamics, and suggest that intrahost ZIKV mutations capable of augmenting fitness in pregnant vertebrates may not necessarily spread efficiently via mosquitoes during epidemics.IMPORTANCEAlthough Zika virus infection of pregnant women can result in congenital Zika syndrome, the factors that cause the syndrome in some but not all infected mothers are still unclear. We identified a mutation that was present in some ZIKV genomes in experimentally inoculated pregnant rhesus macaques and their fetuses. Although we did not find an association between the presence of the mutation and fetal death, we performed additional studies with it in non-pregnant macaques, pregnant mice, and mosquitoes. We observed that the mutation increased the ability of the virus to infect mouse fetuses but decreased its capacity to produce high levels of virus in the blood of non-pregnant macaques and to be transmitted by mosquitoes. This study shows that mutations in mosquito-borne viruses like ZIKV that increase fitness in pregnant vertebrates may not spread in outbreaks when they compromise transmission via mosquitoes and fitness in non-pregnant hosts.

scholarly journals The risk of urban yellow fever resurgence in Aedes-infested American cities

2018 ◽  
Vol 146 (10) ◽  
pp. 1219-1225 ◽  
Author(s):  
Eduardo Massad ◽  
Marcos Amaku ◽  
Francisco Antonio Bezerra Coutinho ◽  
Claudio José Struchiner ◽  
Luis Fernandez Lopez ◽  
...  
Keyword(s):  
Yellow Fever ◽  
Urban Areas ◽  
Endemic Area ◽  
Unit Area ◽  
Vector Competence ◽  
Eradication Programme ◽  
Sylvatic Cycle ◽  
Force Of Infection ◽  
American Cities ◽  
Urban Cycle

AbstractAedes aegypti, historically known as yellow fever (YF) mosquito, transmits a great number of other viruses such as Dengue, West Nile, Chikungunya, Zika, Mayaro and perhaps Oropouche, among others. Well established in Africa and Asia, Aedes mosquitoes are now increasingly invading large parts of the American continent, and hence the risk of urban YF resurgence in the American cities should because of great concern to public health authorities. Although no new urban cycle of YF was reported in the Americas since the end of an Aedes eradication programme in the late 1950s, the high number of non-vaccinated individuals that visit endemic areas, that is, South American jungles where the sylvatic cycle of YF is transmitted by canopy mosquitoes, and return to Aedes-infested urban areas, increases the risk of resurgence of the urban cycle of YF. We present a method to estimate the risk of urban YF resurgence in dengue-endemic cities. This method consists in (1) to estimate the number of Aedes mosquitoes that explains a given dengue outbreak in a given region; (2) calculate the force of infection caused by the introduction of one infective individual per unit area in the endemic area under study; (3) using the above estimates, calculate the probability of at least one autochthonous YF case per unit area produced by one single viraemic traveller per unit area arriving from a YF endemic or epidemic sylvatic region at the city studied. We demonstrate that, provided the relative vector competence, here defined as the capacity to being infected and disseminate the virus, of Ae. aegypti is greater than 0.7 (with respect to dengue), one infected traveller can introduce urban YF in a dengue endemic area.

scholarly journals Low vector competence in sylvatic mosquitoes limits Zika virus to initiate an enzootic cycle in South America

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Rosilainy S. Fernandes ◽  
Maria I. Bersot ◽  
Marcia G. Castro ◽  
Erich Loza Telleria ◽  
Anielly Ferreira-de-Brito ◽  
...  
Keyword(s):  
South America ◽  
Zika Virus ◽  
Vector Competence ◽  
Mosquito Species ◽  
Vital Role ◽  
Infection Rates ◽  
Viral Isolate ◽  
Viral Dissemination ◽  
Transmission Cycle ◽  
Genetically Determined

AbstractZika virus (ZIKV) has spread in the Americas since 2015 and the potential establishment of a sylvatic transmission cycle in the continent has been hypothesized. We evaluated vector competence of five sylvatic Neotropical mosquito species to two ZIKV isolates. Distinct batches of Haemagogus leucoceleanus, Sabethes albiprivus, Sabethes identicus, Aedes terrens and Aedes scapularis females were respectively orally challenged and inoculated intrathoracically with ZIKV. Orally challenged mosquitoes were refractory or exhibited low infection rates. Viral dissemination was detected only in Hg. leucocelaenus, but with very low rates. Virus was not detected in saliva of any mosquito orally challenged with ZIKV, regardless of viral isolate and incubation time. When intrathoracically injected, ZIKV disseminated in high rates in Hg. leucocelaenus, Sa. identicus and Sa. albpiprivus, but low transmission was detected in these species; very low dissemination and no transmission was detected in Ae. terrens and Ae. scapularis. Together these results suggest that genetically determined tissue barriers, especially in the midgut, play a vital role in inhibiting ZIKV for transmission in the tested sylvatic mosquito species. Thus, an independent enzootic transmission cycle for ZIKV in South America is very unlikely.

scholarly journals Starvation at the larval stage increases the vector competence of Aedes aegypti females for Zika virus

2021 ◽  
Vol 15 (11) ◽  
pp. e0010003
Author(s):  
Christie S. Herd ◽  
DeAna G. Grant ◽  
Jingyi Lin ◽  
Alexander W. E. Franz
Keyword(s):  
Aedes Aegypti ◽  
Salivary Glands ◽  
Blood Meal ◽  
Zika Virus ◽  
Vector Competence ◽  
Transmission Cycle ◽  
Physical Evidence ◽  
Transmission Electron ◽  
Primary Vector ◽  
Blood Meal Digestion

Aedes aegypti is the primary vector of Zika virus (ZIKV), a flavivirus which typically presents itself as febrile-like symptoms in humans but can also cause neurological and pregnancy complications. The transmission cycle of mosquito-borne arboviruses such as ZIKV requires that various key tissues in the female mosquito including the salivary glands get productively infected with the virus before the mosquito can transmit the virus to another vertebrate host. Following ingestion of a viremic blood-meal from a vertebrate, ZIKV initially infects the midgut epithelium before exiting the midgut after blood-meal digestion to disseminate to secondary tissues including the salivary glands. Here we investigated whether smaller Ae. aegypti females resulting from food deprivation as larvae exhibited an altered vector competence for blood-meal acquired ZIKV relative to larger mosquitoes. Midguts from small ‘Starve’ and large ‘Control’ Ae. aegypti were dissected to visualize by transmission electron microscopy (TEM) the midgut basal lamina (BL) as physical evidence for the midgut escape barrier showing Starve mosquitoes with a significantly thinner midgut BL than Control mosquitoes at two timepoints. ZIKV replication was inhibited in Starve mosquitoes following intrathoracic injection of virus, however, Starve mosquitoes exhibited a significantly higher midgut escape and population dissemination rate at 9 days post-infection (dpi) via blood-meal, with more virus present in saliva and head tissue than Control by 10 dpi and 14 dpi, respectively. These results indicate that Ae. aegypti developing under stressful conditions potentially exhibit higher midgut infection and dissemination rates for ZIKV as adults, Thus, variation in food intake as larvae is potentially a source for variable vector competence levels of the emerged adults for the virus.

scholarly journals Fetal globin expression in New World monkeys.

1996 ◽  
Vol 271 (47) ◽  
pp. 30298
Author(s):  
Robert M. Johnson ◽  
Steven Buck ◽  
Chi-hua Chiu ◽  
Horacio Schneider ◽  
Iracilda Sampaio ◽  
...  
Keyword(s):  
New World ◽  
New World Monkeys

scholarly journals Association between Genetic Variants in NOS2 and TNF Genes with Congenital Zika Syndrome and Severe Microcephaly

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 325
Author(s):  
Julia A. Gomes ◽  
Eduarda Sgarioni ◽  
Juliano A. Boquett ◽  
Ana Cláudia P. Terças-Trettel ◽  
Juliana H. da Silva ◽  
...  
Keyword(s):  
Risk Factors ◽  
Zika Virus ◽  
Genetic Variants ◽  
Educational Level ◽  
Congenital Anomalies ◽  
Family Income ◽  
First Trimester ◽  
In Utero ◽  
Zikv Infection ◽  
Congenital Zika Syndrome

Zika virus (ZIKV) causes Congenital Zika Syndrome (CZS) in individuals exposed prenatally. Here, we investigated polymorphisms in VEGFA, PTGS2, NOS3, TNF, and NOS2 genes as risk factors to CZS. Forty children with CZS and forty-eight children who were in utero exposed to ZIKV infection, but born without congenital anomalies, were evaluated. Children with CZS were predominantly infected by ZIKV in the first trimester (p < 0.001) and had mothers with lower educational level (p < 0.001) and family income (p < 0.001). We found higher risk of CZS due the allele rs2297518[A] of NOS2 (OR = 2.28, CI 95% 1.17–4.50, p = 0.015). T allele and TT/CT genotypes of the TNF rs1799724 and haplotypes associated with higher expression of TNF were more prevalent in children with CZS and severe microcephaly (p = 0.029, p = 0.041 and p = 0.030, respectively). Our findings showed higher risk of CZS due ZIKV infection in the first trimester and suggested that polymorphisms in NOS2 and TNF genes affect the risk of CZS and severe microcephaly.

Sign in / Sign up

Export Citation Format

Share Document