In 2014, Central and South America experienced a never-before-seen Zika virus epidemic. Climate and environmental conditions may have played a role in the transmission and rapid spread of the virus throughout the continent. How then, did an
African endemic virus spread virtually undetected through the Americas in such a short space of time?
The Zika virus was first discovered in 1947 in a macaque in Uganda and was eventually reported in Micronesia, an island in the Western Pacific region, between 2007 and 2014. During this time, the Zika virus was considered a mild disease
with relatively small outbreaks. Infection results from the transmission of the virus through the Aedessp. mosquito bites, and symptoms of infections are usually mild, including a rash, headache, conjunctivitis and muscle
The news of Zika first arriving in the Americas came to light in May 2015. Not long after, the epidemic spread to many countries in South America, Central America and even the Caribbean.
This new development was worrisome, as it affected over 100 million people by 2016 and it was revealed that a Zika virus infection in pregnant women could cause foetal congenital malformations and microcephaly (small heads and
Zika virus enters the Americas
So, how did this African arbovirus enter the continent? Epidemiological studies claim the Zika virus entered the Americas as early as 2013. Phylogenetic analysis suggested, however, that the Zika virus possibly entered the Americas from the
Pacific islands, after an outbreak in French Polynesia in 2013, since they were found to come from the same Asian-genotype lineage. But how exactly did this occur? It is difficult to know with certainty, but some have suggested that
increased air travel of passengers carrying the virus to Brazil from the Pacific Islands may be a possibility.
‘The Zika virus entered the Americas as early as 2013.’
Later, towards the end of 2014 and early 2015, a Zika virus epidemic emerged in Manaus, Brazil. The first PCR-confirmed case was identified in November 2015, this means the disease spread undetected for a few years before it was eventually
discovered. Research later determined that Zika cases in the Amazon region of Manaus had resulted from a single introduction event in 2013.
Genomic sequencing of the virus promoted the idea of a single introduction since 93% of samples (55 out of 59) from Manaus come from a single common viral ancestor. This indicates that this single introduction, followed by three epidemic
waves, were responsible for the large epidemic in Manaus during 2015.
Even if the virus was indeed present in 2013, it may have taken up to 2015 and the biannual variability of transmission to create the epidemics that consequently hit the country,
Journey to Central America and Mexico
Genomic epidemiology was used to reconstruct the journey of the Zika virus from Brazil into Central America via Honduras. This journey may have occurred in the summer of 2014 (August to September) and the following research has shed light
on a theory as to how this happened.
‘Genomic epidemiology was used to reconstruct the journey of the Zika virus from Brazil into Central America via Honduras.’
In the summer of 2014, a viral strain from a Honduran who became ill with Zika fever revealed evidence of strains circulating in Brazil. The Zika virus was thus spread from Honduras to its neighbouring countries of Guatemala and Nicaragua
in late 2014, finally reaching Mexico in early 2015.
But how could this occur so quickly? How can a virus that had never been seen before in the Americas travel through the entirety of Central America, from Brazil to Mexico, just within a year or so?
The evidence suggests that the rapid virus spread was made possible due to the presence of an endemic vector to transmit the virus (the mosquito), the ideal climate conditions for disease transmission and a particular biannual trend of Zika
The perfect storm?
The Zika virus seems to be highly suited to the tropical climate of South America, Central America and Mexico, as well as for its endemic vectors (Aedes sp.). The Aedes mosquito, which is endemic to these regions, is known to transmit dengue
and chikungunya viruses, and generally, be the cause of regular outbreaks.
Additionally, climate data from weather stations in Manaus showed the climate conditions around this time may have contributed to the transmission of the Zika virus throughout most of 2014. Zika virus and its vector, much like the dengue
virus, have an association with temperature and precipitation since the ideal transmission conditions for Zika is approximately 29°C (22.7 to 34.7°C).
Due to this relationship, Zika cases are expected to rise due to climate change, seasonality and urbanisation. It is also possible that warmer temperatures may affect the mosquitoes that are most infectious and extend the vector's lifespan.
Even though genomic analysis points to the virus having already been circulating for the previous five years, it may have been the climatic conditions of this specific time and place which allowed the epidemic to become dominant enough to
spread to other countries.
The Zika epidemics may have spread so quickly due to biannual trends of transmission observed during 2014 and 2015, which researchers may not have anticipated. This was due to an observation that the transmission of the Zika virus occurred
in two waves, spreading in both winter and summer. Additionally, epidemics peaked every six months, rather than once a year. This may explain why in 2015, Honduras suffered two epidemic peaks, which correspond with outbreaks in neighbouring
‘The evidence suggests that the virus spread was made possible due to biannual trends of Zika transmission.’
The reason for this rapid spread was linked to the climatic suitability of the Aedes mosquito in these countries and the peculiar pattern of Zika transmission. However, more questions remain about the environmental factors that played a
role in the emergence of Zika in Central America around 2014.
Environmental factors at play?
Indeed the increase of temperatures brought about by climate change in recent history is increasing the transmission rates of mosquito-borne diseases in South and Central America. Despite this established association with temperature, there
may be other ecological factors at play in the increased vulnerability of Central America.
Deforestation, forest degradation and urbanisation are some of the anthropogenic activities associated with this vulnerability. In the last two decades, these factors have shrunk the forests of Central America by 23%, worryingly affecting
indigenous populations and biodiversity.
Some of the socioeconomic drivers of deforestation include modern transportation infrastructure, agricultural practices, illegal logging, cattle ranching and drug trafficking. The latter has led to the clearing of remote areas to create
smuggling routes, as Central America is the primary route for cocaine into North America, approximately accounting for 86% of global worldwide cocaine trafficking.
The invasion of natural spaces and the possible occurrence of sylvatic cycles (the natural transmission cycles of a pathogen) between non-human primates and mosquitoes cannot be ruled out. However, more evidence is needed to confirm this;
there are three primate species in Central and South America known to have some susceptibility to Zika virus infection: Nancy Ma’s night monkeys (Aotus nancymaae), Guianan squirrel monkeys (Saimiri sciureus) and black-tufted
marmosets (Callithrix penicillata).
Having pointed out many reasons for how the Zika virus entered the Americas, its rapid spread most likely resulted from human mobilisation, together with the environmental and climatic conditions that promoted the increased population of
the Aedes vector.
‘There are three primate species in Central and South America known to have some susceptibility to Zika virus infection.’
So, how did an African arbovirus take South and Central America by storm within just one year? This question is still very difficult to answer and more epidemiological research is needed to better understand how the Zika virus journeyed
from Brazil to Mexico. It would also be useful to discover how other factors, such as sexual transmission and herd immunity, played a role in the epidemic. Additionally, Zika virus cases were over-reported in many locations, heightening
awareness and panic regarding the link between Zika virus and microcephaly.
Central and South America should pay close attention and understand how all this was possible in such a short period. Doing so would help the continent to prepare for the next deadly infectious disease and ideally keep cases, disabilities
and deaths to a minimum.
Faria N.R., Azevedo R.D., Kraemer M.U., et al. (2016) Zika virus in the Americas: early epidemiological and genetic findings. Science.Volume 352, Issue 6183, pages 345-349
Giovanetti M., Rodrigues Faria N., Lourenço J., et al. (2020) Genomic and Epidemiological Surveillance of Zika Virus in the Amazon Region. Cell Reports. Volume 30, Issue 7, pages 2275-2283.
Goutam C., Devaleena M. (2022) Chapter 35 - Effect of climate change on mosquito population and changing pattern of some diseases transmitted by them. Advances in Animal Experimentation and Modeling. Pages 455-460.
Kazmi S.S., Ali W., Bibi N. et al. (2020) A review on Zika virus outbreak, epidemiology, transmission and infection dynamics. J of Biol Res-Thessaloniki.Volume 27, number 5.
Musso D. and Gubler D.J (2016) Zika Virus. Clinical Microbiology Reviews. Volume 29, Issue 3, pages 487-524.
Ortiz D.I., Piche-Ovares M., Romero-Vega L.M., Wagman J., Troyo A. (2022) The Impact of Deforestation, Urbanization, and Changing Land Use Patterns on the Ecology of Mosquito and Tick-Borne Diseases in Central America.
Insects. Volume 13, issue 1, page 20.
Tesla B., Demakovsky L.R., Mordecai E.A., et al (2018) Temperature drives Zika virus transmission: evidence from empirical and mathematical models. Proc. R. Soc. Volume 285, issue 1884, 20180795.
J., Li T, du Plessis L., et al (2018) Genomic Epidemiology Reconstructs the Introduction and Spread of Zika Virus in Central America and Mexico. Cell Host & Microbe. Volume 23, Issue 6, pages 855-864.