With the outbreak of Zika virus (ZIKV) from 2013 to 2015, although there were clinical evidence regarding pregnant patients with ZIKV gives birth to birth defected infants, there weren’t experimental evidence of how this virus causes birth defects. Therefore to understand whether a specific type of ZIKV affects the embryo this research dig deep into how the ZIKV strain causes birth defects. Due to previous research, it was already known out of all the different strains of ZIKV, the Brazilian ZIKV strain causes the most severe congenital malformations. In order to understand how ZIKV was affecting the fetus, the location of the ZIKV mostly found in the body needs to be identified. Figure 1 identified the difference in fetal mice born from …show more content…
Figure 2 shows the result from transmission electron microscope, immunostaining, and fluorescence -activated cell analyses (FAC) for Mock, Brazilian ZIKV, and African ZIKV. First finding was between Mock and the Brazilian ZIKV and African ZIKV there were higher NPCs detected in the mock than neurons for AXL and MERTX receptor but when observed in Brazilian ZikV and African ZiKV infected pup, NPC and neurons were equivalent. Comparing the NPCs production in all three sets of cells with brazilian ZIKV showed increase of ZIkV RNA within the NPCs supernatant. But not the NPCs of African strain. The neuron cells were equivalent rate for both strains. Cell deaths were greatly observed in NPCs cultures than the neurons. Overtime sizes of all three NPC influenced neurosphere were measured. The result shows decrease in size for African and brazilian ZIKV and this supports brazilian ZIKV induces cell death in NPCs instead of neurons. For second part 2i and 2j since African ZIkV isn't as severe as Brazillian strain in the second part of the experiment cell death seems to decrease over time suggesting something is probably preventing apoptosis. What is it? Further comparison with African strain and Brazilian strain to understand their difference to lower the severe condition of microcephaly. As discussed before since infants are usually born with cortical development, the subtypes of cortical neurons amounts at 24 and 96 hours get investigated using organoids grow
First isolated from a rhesus monkey in Uganda, the Zika virus (ZIK V) did not pose a serious global threat until recent outbreaks in 2007 on Yap Island in Micronesia and the current outbreak which began in 2013 in the French Polynesia. And, although the virus is transmitted via infected mosquitoes, studies indicate that the disease potentially can be transmitted sexually (Musso, D., Roche, C., Robin, E., Nhan, T., Teissier, A., and
This result has been 30 times higher than pre-Zika virus years and there has been more birth defect within the first trimester. The result of the study indicated that 15% of women with confirmed Zika infection during the first trimester had babies with birth defects and that almost every state reported one woman with suspected Zika infection during pregnancy. Based on the report, infants born to women with evidence of possible Zika virus infection should follow-up and routine development assessment that will help identify for future outcomes associated with the Zika virus. Neuroimaging test is needed to detect these abnormalities. The report also indicates that the study has at least four limitations and that there was limited data about the maternal risk factors such as genetic or other infectious causes, which could has been the reason for some of the birth defects reported in the study. Overall, the result of this study is important because it gives more information about the Zika virus and how is affecting pregnant women in U.S.
McNeil, Donald G., and Pam Belluck. "Extensive Brain Defects seen in Babies of Mothers with Zika." New York Times, 14 Dec, 2016, pp. A.3, SIRS Issues Researcher, https://sks.sirs.com.
The start of the video explains the origin of the propagation of the Zika virus, which uses the Aedes mosquito as a host, to aid in the dispersion of the virus by method of biting. Once the person has been bitten by the mosquito and contract Zika, the virus can continue to disseminate through sexual contact or from a pregnant woman to her fetus. The Center for Disease Control and Prevention (CDC) arrived to an important conclusion, Zika virus causes many malformation
The Zika virus has had a constant presence in the news for the past few months. This article describes Ana Gabriela do Prado Paschoal's struggles. She contracted the Zika virus while pregnant with her now three month old daughter Maria. Maria now suffers from brain lesions, stiff muscles, and brain damage. With the help of scans, imaging, and autopsies doctors learned that the Zika virus eats away at the fetal brain. It is responsible for shrinking or destroying the part of the brain that controls vision, thought process, and other basic functions.
Stein also reports that microcephaly in infants due to the Zika virus is rare, but the risk has been increased in Brazil, due to the endemic status of the infection (Stein, 2016). This article mainly focuses on pregnant women and their children,
Since then, the Zika virus has been rapidly spreading in Brazil and other Latin American and Caribbean countries. On Feb. 1, 2016, the Zika virus was announced as a public health urgency by the World Health Organization (WHO), and the virus was linked to the microcephaly in which babies are born with a brain defect (Tavernise, 2016). The Zika is not a deadly disease, and the symptoms are: fever, rash, inflamed eyes, and joint pain (Ramzy, 2016). However, one significant effect of the Zika virus is the microcephaly because a baby with microcephaly has abnormally small head which includes brain, eyes, and ears, damages (CDC, 2016). It is not only the baby’s life that is effected but also the parent’s lives will be changed because the parents have to take care of the baby for the rest of their lives. More than 3,800 infants in Brazil have recently been found to have microcephaly (Romero, 2016). The Zika epidemic has spread 25 countries (Jacob, 2016); however, why is the Zika epidemic growing more serious in Brazil? The Zika epidemic has been attributed to some factors, including: the Aedes aegypi mosquitoes’ habitats, the
i) A study done in Brazil showed that as many as 30% of babies born to women who had been infected with Zika showed signs of microcephaly, that is, an abnormally small head (Baden et al, 1556) ii) Microcephaly limits the development of infants’ brain before birth, and is associated with seizures, learning disorders, developmental delays, and vision and hearing loss (Schmidt,
While Zika can cause new borns to be born with astringent brain affliction, there may be an opportunity to tame the virus to fight brain tumors in adults. The Zika virus, which landed in South America from Polynesia about four years back, is most hazardous in pregnant ladies. It can cause microcephaly and related neurological issues in the children of ladies who were contaminated while pregnant, also with a higher rate of a miscarriage.
Zika is a virus with no vaccine and no cure that can cause Microcephaly. Microcephaly is when a child’s brain has not developed properly and he or she is born with an abnormally small head.
The zika is a member of Flaviviridae family and the virus is transmitted via mosquito to humans and the findings of the experiments done by Dr. Kellie Ann Jurado and her team are extremely important for modern society since it’s a major health problem that even affected Floridian residents. Sika virus has caused a recent epidemic and spread in the Americas. The zika virus is not a new virus but only recently is has being more studied it was isolated from monkeys in 1947. The spread of the zika was relatively silence since the pathogenic consequences it cause were not as great as other viruses. When the sika virus hit the Americas a large group of scientists and Dr. Kellie Ann Jurado included started to see
Neural progenitor cells are permissive of Zika virus (ZIKV) infection in humans, and the ZIKV’s ability to infect such cells is a major global concern, because no other virus from the Flaviviridae family can infect brain cells. AXL was identified as the virus’s mediator for entry and disruption of radial glial cells and endothelial cells of the brain. To analyze the virus- host interaction, specifically the reprograming of the host proteins directed by AXL after Zika entry, the study of the effect of ZIKV infection on the epigenome in mouse radial glial cells is to be performed. To visualize the epigenetic changes caused by the virus the mapping of the epigenome of both infected and mock RGC cells is done. Whole ZIKV-infected E17.5 fetal brains
Scientist suspect that the mutation in the Zika virus, that causes the abnormally small sized heads and brains of babies, first showed up in 2013. Discovered decades ago the Zika virus is spread by mosquitoes, but wasn’t linked to high rates of microcephaly (a birth defect where a baby's head is smaller than expected when compared to other babies) until recently. Researchers, unsure as to why the birth defects were being caused by the virus, originally thought that it might have been the immune system of the people in South American that was causing the problems but a researcher, Shi, and a team in China hypothesized that these changes, were brought about by a change or mutation in the Zika virus.
The recent emergence and the spread of Zika virus (ZIKV) in several countries around the globe have been considered as an emerging global public health problem. ZIKV is an arbovirus belongs to the flavivirus genus. ZIKV is an enveloped, spherical virus containing a single-stranded positive RNA with a genome consisting of approximately 10,794 nucleotides. The RNA of ZIKV is translated into a polyprotein which is co & post-translationally cleaved into 11-mature proteins. ZIKV was first identified in the Zika forest of Uganda in 1947 (1). ZIKV is primarily transmitted by the infected Aedes mosquito’s bites (2), and resides in the salivary glands of infected mosquitoes. ZIKV is, also, found to be sexually transmitted as the ZIKV RNA, have been observed in sperm and urine after 62days of infection (3,4). In
To characterize ZIKV replication in the context of pre-existing immunity against DENV or WNV during pregnancy, we measured viral loads in the blood and several maternal organs, including the brain, spleen, and spinal cord. Quantification of ZIKV RNA in the blood on day 3 postinfection showed a trend towards increased viremia for both DENV- and WNV-immune plasma conditions, although these differences were not significant (Fig. 2A). Increased viremia was not as evident as we previously described (12) despite equal levels of circulating human IgG (Fig. S2). This was most likely due to immune changes caused by pregnancy, as well as the increased age of