Bacteria prevent transmission of Zika and Dengue viruses

Scientists at the University of Glasgow's MRC Centre for Virus Research opens in new window (CVR) have found a bacterial strain which blocks dengue and Zika virus transmission from mosquitoes. In a new study, published in PLOS Pathogens opens in new window, the scientists show that a novel strain of the inherited bacteria, called Wolbachia, strongly blocks transmission of dengue and Zika virus in infected mosquitoes. This finding could offer a potential alternative to strains already being tested as virus control tools.

The scientists have already carried out the research in the mosquito species Aedes aegypti, notorious for spreading several dangerous human viruses, including dengue, Zika and chikungunya. Previous research in the scientific community has shown that transmission of these viruses among mosquitoes is stalled if the flies are deliberately infected with one strain of Wolbachia bacteria. With this knowledge, several countries are testing whether infecting local mosquito populations with Wolbachia could lead to lower rates of viral disease in humans.

The MRC scientists in Glasgow found that a novel strain-called 'wAu' – is more effective for virus transmission blocking than the strains currently being used. The effect is emphasised in hot, tropical climates where there is a high prevalence of these diseases. The Wolbachia transmission blocking strategy shows great promise for the control of mosquito-borne viruses, and is now starting to be deployed on a large scale in a number of tropical countries.

The results with the wAu strain showed by far the effective transmission blocking for all the viruses we tested, and it provides an exciting new option to explore for disease control programmes. Several Wolbachia strains have already been tested in the field, but there is evidence to suggest that some strains may not block transmission very effectively or may not be inherited efficiently at high ambient temperatures. In the new study, the research team performed laboratory experiments to test the potential promise of alternative Wolbachia strains.

The researchers introduced four Wolbachia strains into Aedes aegypti mosquitoes, which do not naturally carry these anthropod-infecting bacteria. Two of the strains, wMel and wAlbB had already been evaluated in prior studies, and the scientists wanted to compare their effects with those of two novel strains, wAu and wAlbA.

The analysis revealed particularly promising results for strain wAu. After feeding on blood infected with dengue or Zika virus, mosquitoes infected with wAu had lower levels of viral RNA in their body tissue than did mosquitoes infected with the other strains. wAu also showed very high rates of inheritance, including under high-temperature conditions. The aim is to reduce and block the transmission of pathogens by releasing specific insect disease vectors.
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Repurposed drug effective for Zika virus

In both cell cultures and mouse models, a drug used to treat Hepatitis C effectively protected and rescued neural cells infected by the Zika virus and blocked transmission of the virus to mouse fetuses. Researchers at University of California San Diego School of Medicine, with colleagues in Brazil and elsewhere, say their findings support further investigation of using the repurposed drug as a potential treatment for Zika-infected adults, including pregnant women.

 Zika infection during the first trimester confers the greatest risk of congenital microcephaly. Outbreaks of Zika virus in Brazil in 2015 and 2016 were marked by an increased incidence of newborns with congenital malformations, most notably undersized heads (microcephaly) and significant neurological abnormalities.

A great deal of research has focused on the pathology of Zika infections, including earlier work by the Muotri lab and collaborators that described how the virus is transmitted from mother to fetus by infecting cells that, ironically, will later develop into the brain's first and primary form of defense against invasive pathogens.

In its latest work, however, the Muotri lab sought clinical solutions. The team investigated an antiviral drug called sofosbuvir, approved and marketed under the brand name Sovaldi to treat and cure hepatitis C infections. The drug works by inhibiting replication of the hepatitis C virus; researchers noted that both hepatitis C and Zika belong to the same viral family and bore strong structural similarities that could make sofosbuvir effective against the latter. In addition, it had been reported that sofosbuvir was protective against Zika in different cell types.

In tests using human neural progenitor cells (NPCs)-self-renewing, multipotent cells that generate neurons and other brain cell types-the scientists found that exposure to sofosbuvir not only rescued dying NPCs infected with the Zika virus, but restored gene expression linked to their antiviral response. In subsequent tests using an immunodeficient mouse model infected by Zika, intravenous injections of sofosbuvir significantly reduced viral loads in blood serum compared to a placebo group.

Fetuses of Zika-infected pregnant mice did not show detectable Zika virus amplification in the sofosbuvir-treated group. This shows that the drug was well-tolerated by the Zika-infected pregnant mice and that it was able to arrest Zika replication in vivo and stop transmission from mother to fetus.
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Zika virus damages placenta

Zika virus is known for a recent outbreak that caused children to be born with microencephaly, or having a small head, and other malformations, new research suggests the virus damages a pregnant mother's placenta, an organ inside a woman's uterus that protects and cares for a growing baby.

Zika virus infection in five pregnant rhesus monkeys caused placental tissues to become thickened and inflamed. As a result, the researchers saw less oxygen being transported across the placenta and to the baby. Decreased oxygen levels in a placenta can impair fetal development and ultimately the health of a baby.

The role of a placenta is to protect and provide nutrition to a growing baby for optimum health Professor Daniel Streblow, Ph.D., and assistant professor Alec Hirsch, Ph.D., both of whom lead molecular microbiology and immunology research at the OHSU Vaccine and Gene Therapy Institute. Streblow also leads pathobiology and immunology research at the Oregon National Primate Research Center and is a professor of molecular microbiology and immunology within the OHSU School of Medicine.

The reseachers used a non-invasive, in vivo MRI technique to evaluate oxygen levels inside the placenta and oxygen flow between mother and baby. They found that, in monkeys that were infected with Zika early in their pregnancies, the rate of oxygen transport through the placenta decreased about 10-fold. The OHSU research team also determined the Zika virus can readily pass from mother to baby and remain in the baby long-term, leading to a chronic infection in utero.

 These findings may provide important insights into the mechanisms by which Zika virus causes disease during pregnancy. By better understanding how both mother and child become infected with and affected by the Zika virus, researchers can determine how to prevent its infection and disease. The OHSU research team is using the knowledge gained from this study to develop a safe and effective Zika vaccine for use during pregnancy.
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How Zika virus induces congenital microcephaly

Epidemiological studies show that in utero fetal infection with the Zika virus (ZIKV) may lead to microcephaly, an irreversible congenital malformation of the brain characterized by an incomplete development of the cerebral cortex. However, the mechanism of Zika virus-associated microcephaly remains unclear.

Combined analysis of human fetuses infected with Zika virus, cultures of human neuronal stem cells and mice embryos showed that ZIKV infection of cortical progenitors -stem cells for cortical neurons) controlling neurogenesis triggers stress in the endoplasmic reticulum -where some of the cellular proteins and lipids are synthesized in the embryonic brain, inducing signals in response to incorrect protein conformation.

When it reaches the brain, Zika virus infects neuronal stem cells, which will generate fewer neurons, and by inducing chronic stress in the endoplasmic reticulum, it promotes apoptosis-the early death of these neuronal cells. These two combined mechanisms explain why the cerebral cortex of infected fetuses becomes deficient in neurons and is therefore smaller in size.

 Researchers administered an inhibitors of protein-folding re-sponse in cortical progenitors and found that this inhibited the development of microcephaly in mice embryos infected with Zika virus. The defects observed are specific to an infection by ZIKV, as other neurotropical viruses of the flavivirus family- West Nile virus and yellow fever did not cause microcephaly, in contrast to Zika virus.
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Anti-malarial drug for Zika virus treatment

Medication used to prevent and treat malaria may also be effective for Zika virus. The drug, called chloroquine, has a long history of safe use during pregnancy. Zika causes mild flu-like symptoms. But in pregnant women, the virus can cause serious birth defects in babies-including microcephaly-a neurological condition in which newborns have unusually small heads and fail to develop properly.

Presently, there is no treatment or way to reverse the condition. The latest research suggests the anti-malaria drug chloroquine may be an effective drug to treat and prevent Zika infections. Reseachers examined the effect of chloroquine in human brain organoids and pregnant mice infected with the virus, and found the drug markedly reduced the amount of Zika virus in maternal blood and neural progenitor cells in the fetal brain.

Pregnant mice received chloroquine through drinking water in dosages equivalent to acceptable levels used in humans. Although chloroquine did not completely clear Zika from infected mice it did reduce the viral load, suggesting it could limit the neurological damage found in newborns infected by the virus.
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Naturally acquired immunity against Zika virus

During their study of Zika infection in pregnant mice, the researchers built-up immunity in previously infected mothers that continued into pregnancy and protected fetal tissues. Because the mothers had already cleared their non-symptomatic Zika infections, they developed high levels of protective immunoglobulin antibodies against the virus that researchers found in the animals. Detection of these protective antibodies points to the possibility of developing diagnostic tests to identify naturally immune women and distinguish them from women at high risk of infection.

The ability to identify high-risk women would help develop focused therapeutic strategies for prevention, combining protective antibodies with an eventual vaccine, which could synergistically provide more a robust level of protection against Zika. Built-up immunoglobulin antibodies protect against Zika infection in mothers and their developing fetal offspring.

Researchers said expectant mothers are susceptible to Zika infection compared to non-pregnant women. If the virus is active during pregnancy, it usually spreads to vital tissues of a developing fetus. Because Zika virus infection in healthy non-pregnant women is mostly asymptomatic, many women of reproductive age in high-risk regions have a cleared infection before pregnancy.

Susceptibility to Zika virus infection was markedly reduced in mice that had previously cleared a prior infection compared to those undergoing a first infection during pregnancy. Mice that didn't have prior Zika infections developed clinical symptoms and sharply increased levels of Zika virus in their blood, which spread to fetal tissues.

Zika virus could not be found in most of the baby mice from mothers with resolved infection prior to pregnancy. Protection found in Zika-resistant mice could be transferred to susceptible mice with Zika virus neutralizing antibodies found in the blood of mice with prior asymptomatic infection.
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Dengue immunity can protect against Zika

Manifestations of Zika virus (ZIKV) infection differ drastically. Sometimes they are catastrophic, most notably when they cause microcephaly in some babies born to infected mothers. At other times, they are mild and fleeting, suggesting that unknown factors temper Zika infections' severity.

Recently, dengue virus emerged as a prime suspect because it shares many genetic and structural characteristics with ZIKV and is endemic in most of the regions affected by Zika's global spread.
Mice rendered immune to dengue show "cross-protection" from subsequent Zika infection and then identifies specific types of immune T-cells capable of defending against both viruses.

These revelations have profound implications for efforts to build a potent anti-Zika vaccine. In some parts of the world Zika is almost like a secondary infection. It has spread into Brazil/Latin America and is moving into places in Asia where people previously had dengue. Vaccines targeting either virus could be engineered to induce both T cell and antibody responses effective to protect people in these areas.

When one encounters a pathogen in real life, two arms of the immune system spring into action to neutralize it. In the so-called humoral response, B-cells begin to secrete specific antibody proteins, which latch onto and neutralize pathogens in tissue or blood. Simultaneously, a cell-mediated immunity system also becomes active, deploying cytotoxic T-cells to directly recognize and kill pathogen-infected cells.

The ideal vaccine might mimic both antibody and T cell responses to block an infectious disease. But in truth, most (26 of 28 vaccines currently licensed for human use) stimulate primarily a B-cell or antibody response, which in many cases is sufficient. Reseache team created the first "sequential" mouse model mimicking dengue-then-Zika infection. To do that, they infected mice genetically vulnerable to this family of viruses with dengue virus.

Those mice became sick, recovered from infection, and hence acquired immunity to dengue, presumably because viral infection had mobilized their immune B-cells, T-cells or both. The group then inoculated the same mice with ZIKV and waited to see if mice showed ZIKV symptoms. But overall, mice that had previously acquired dengue immunity showed protection against Zika, as evidenced by a reduced burden of ZIKV in blood and tissues, such as brain, liver or testis, compared to control mice not "pre-inoculated" against dengue.

These experiments suggest that the reason that some people infected with Zika do not come down with disease is due to prior exposure to dengue. This may explain why Zika is not passed to the unborn child of every pregnant woman in dengue-endemic countries exposed to virus. In a different experiment, the scientists isolated cytotoxic T cells from the blood of dengue-immune mice and infused them into normal mice, a procedure known as adoptive T-cell transfer.

 When infused mice were then infected with ZIKV, they also showed disease resistance, supporting the idea that the T-cell arm of the immune system can do the heavy lifting against ZIKV infection. A successful vaccine would need to include components to induce not only a B-cell response but also a T-cell response.
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How Zika virus infects developing brain

Zika virus is transmitted from mother to fetus by infected cells that later develop into the brain's first and primary form of defense against invasive pathogens. During embryogenesis- the early stages of prenatal development cells called microglia form in the yolk sac and then disperse throughout the central nervous system CNS of the developing fetus.

In the brain, these microglia will become resident macrophages whose job is to constantly clear away plaques, damaged cells and infectious agents. The Zika virus can infect these early microglia, moving into the brain where they transmit the virus to other brain cells, leading to devastating neurological damage.

The Zika virus is transmitted to people through the bite of infected Aedes species mosquitoes. However, a pregnant woman can also pass the virus to her fetus, the researchers used human induced pluripotent stem cells to create two relevant CNS cell types: microglia and neural progenitor cells (NPCs), which generate the millions of neurons and glial cells required during embryonic development.

Then they established a co-culture system that mimicked the interactions of the two cell types in vitro when exposed to the Zika virus. They discovered that the microglia cells engulfed Zika-infected NPCs, doing their job. But when these microglia carrying the virus were placed in contact with non-infected NPCs, they transmitted the virus to the latter.
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DNA - based Zika vaccine is safe

Zika virus is a mosquito-borne infection associated with birth defects and neurological complications in adults. However, no approved vaccine or treatment is currently available for treatment of Zika virus. A new generation DNA-based Zika vaccine demonstrated both safety and ability to elicit an immune response against Zika in humans in a phase 1 clinical trial.

Synthetic DNA vaccines are an ideal approach for infectious diseases like Zika, this new generation of DNA vaccines can be designed and manufactured rapidly, they appear to be highly predictable for the generation of immunity in humans, having significant conceptual safety advantages, and they are more stable than some of the traditional vaccines, making them exceptionally practical to distribute during outbreaks, especially in regions where resources are limited.

The GLS-5700 vaccine contains the synthetic DNA instructions for the host to learn how to mount an immune response against a specific Zika virus antigen. Researchers enrolled some participants in the safety trial, two groups of different participants received two different doses of the vaccine candidate intradermally at zero, four, and 12 weeks.

 Each dosage was followed by Cellectra delivery which generates small, directional electric currents into the skin to facilitate optimal vaccine uptake, production of the intended antigen, and immune responses. Results showed that two weeks after the final dose 100 percent of study participants developed Zika-specific antibodies and 80 percent developed significant neutralizing antibodies against the virus.

Serum from the study participants was able to protect immunocompromised mice from developing the disease after infection with Zika virus, showing that the vaccine-induced antibodies can prevent infection in living organism. Result of this research showed that DNA vaccine can produce an immune response against the virus with minimal adverse effects.
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Zika kills brain cancer stem cells

Zika virus is a mosquito-borne infection known for causing birth defects in unborn fetuses. Latest research discovered that it is possible to use the virus to target tumor cells in adult brains. Combining Zika virus with chemotherapy and radiation can be use to remove brain tumors.

Glioblastoma is the most common and deadly forms of brain cancer with patients dying within two years of diagnosis. The growth and development of glioblastomas is driven by stem cells that proliferate and give rise to other tumor cells.

Stem cells of the cancer are hard to kill because they avoid body's immune system and are resistant to chemotherapy and radiation. Killing these cells is very important to prevent new tumors from recurring after the original tumor has been surgically removed.

 Glioblastoma can occur in any part of the brain, when glioblastoma is diagnosed, microfibers can spread to the rest of the brain which magnetic resonance imaging MRI would not detect. It is common in men between the age of 50 and 60, and there is no link between developing glioblastoma and having a previous cancer history.

Intense exposure to radiation increases the risk of brain cancer. Zika virus disrupts fetal brain development targeting neural stem and progenitor cells, however the virus' effects on adult brains are less severe.

 The preference of Zika virus for neural precursor cells could be leveraged against glioblastoma stem cells, researchers found the virus infected and killed patient-derived glioblastoma stem cells compared with other glioblastoma cell types or normal neural cells.

When mice with aggressive glioblastoma were injected with a mouse-adapted strain of Zika virus, the virus slowed tumor growth and significantly extended the animals' lifespan.

Researchers also tested a mutated strain of Zika on body's immune response, which was more effective when combined with a chemotherapy drug, temozolomide, that usually has little effect on these cells. Zika virus can kill the kind of glioblastoma cells that tend to be resistant to current treatments.
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Zika virus weakened immune system and deformed fetus

The Zika virus increases in pregnant women by suppressing their dampened immune systems and attacks their natural defenses, which allows the virus to directly attack the fetus. A woman's immune system naturally suppresses itself during pregnancy to keep the body from recognizing the fetus as a foreign body and attacking it, Zika uses this process, turning pregnant woman's immune defense so the virus can spread without any hindrance.

Researchers tested African and Asian strains of Zika in the blood samples of healthy men, women and pregnant women. Researchers discovered that the Asian strain of Zika targets monocytes, which are white blood cells that mount the body's immune defense by destroying viruses and bacteria, people can survive the attack, but pregnant women cannot because Zika exploits the existing process by which the body protects a fetus from immune attack. Zika virus suppresses immune system like HIV.

The virus goes in, multiplies, grows and then crosses the placenta attack the fetus and cause disease. The blood of pregnant women infected with Zika also showed abnormally high expression of two genes that have been previously associated with pregnancy complications. Microcephaly have been associated with mothers who were infected with the Zika virus before giving birth, a pregnant women naturally have higher levels of immune-suppressing M2 macrophages to prevent the womb from rejecting the fetus.

However, the Asian Zika virus boosts M2 macrophage reproduction, decreasing the infection fighting process and encouraging immune suppression. Researchers discovered that the Asian Zika virus is more dangerous during first and second trimester, when the virus can increase immune suppression. During the third trimester, the blood of infected pregnant women and non-pregnant women were about the same.

During pregnancy, the host body is prone to opportunistic infection
Previous clinical studies showed that Zika virus infection during the first and second trimesters of pregnancy are strongly associated with fetal abnormalities. These anomalies cause brain damage and developmental delays in babies even if they are born with normal-sized heads.
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Zika may not last in semen as thought

According to the latest research, Zika virus might not remain in the semen of some infected men as long as previously thought.

The researchers said Zika may only be present in semen for about a month. Previous research had suggested that Zika virus can be found in semen for as long as 188 days after the onset of symptoms.

The new study included 12 men in French Guiana who had Zika virus. Four of the men never had any detectable Zika in their semen. One excreted Zika virus in his semen for at least three days. And seven had Zika-laced semen for at least a month.

The maximum duration of detectable Zika in semen in the study was 45 days.
These data suggest that not all men who are symptomatically infected with Zika virus will have Zika virus RNA detectable in semen.

The results also showed that Zika does replicate in the testicles or semen-producing glands, since the amount of Zika in semen was significantly different than the Zika load found in the men's blood.

Zika causes neurological birth defects, most commonly microcephaly, a condition in which a baby's brain and skull are underdeveloped.
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Previous exposure to West Nile may prevents Zika or make it worse

West Nile virus is a mosquito-borne virus that affect many people, previous exposure to this virus can determine the reaction of affected person to Zika virus. Zika virus is a mosquito-borne virus and relative of West Nile.

 Previous exposure to West Nile Virus could either prevents Zika infection or make it worse. The National Institute of Allergy and Infectious Diseases NIAID will collect blood samples from people that had West Nile virus for presence of West Nile antibodies.

 These antibodies would indicate if the individual once had the virus but fought it off. The blood samples of those that had West Nile virus that fought it off in the past will be used to explore antibody-dependent enhancement ADE, where the presence of certain antibodies can either strengthen or fight a subsequent infection.

Researchers will use blood samples that are positive for West Nile antibodies to carry out tests that will determine whether West Nile antibodies enhance or inhibit Zika virus infection.

If the results show that West Nile enhances Zika, people must prevent mosquito bites. If  West Nile inhibits Zika, a vaccine for West Nile could potentially protect against Zika.
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Diagnosing Zika virus with nanotechnology

Testing for Zika requires that a blood sample be refrigerated and moved to a laboratory, this delay diagnosis and treatment. The researchers tested blood samples taken from people infected with Zika virus and compared it to blood from people that do not have the virus.

 Blood from Zika-infected patients tested positive while blood from Zika-negative controls did not. The assay produced no false-positive results.

Zika infection is either asymptomatic or mildly symptomatic; people infected with Zika don't know they're infected, many people don't become sick after being bitten by an infected mosquito.

 Testing is particularly important for pregnant women because Zika infection can cause congenital Zika syndrome, which contributes to several neurologic problems in the fetus or newborn infant.

Population screening is the effective way of diagnosing the diseases. Using of gold nanorods mounted on paper to detect Zika infection within a few minutes is faster and better than the current method.

The test relies on a protein made by Zika virus that causes an immune response in infected individuals. The protein is attached to tiny gold nanorods mounted on a piece of paper.

The paper then is completely covered with tiny, protective nanocrystals. The nanocrystals allow the diagnostic nanorods to be shipped and stored without refrigeration prior to use.

To use the test, a technician rinses the paper with slightly acidic water, removing the protective crystals and exposing the protein mounted on the nanorods. Then, a drop of the patient's blood is applied. If the patient has come into contact with the virus, the blood will contain immunoglobulins that react with the protein.

Immunoglobulins persist in the blood for a few months, and when they come into contact with the gold nanorods, the nanorods undergo a slight color change that can be detected with a hand-held spectrophotometer. With this test, results and treatments will be immediate.
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Zika virus cannot be transmitted by casual contact

Zika virus is a mosquito-borne disease that is spread by the Aedes mosquito,
Casual contact like kissing or sharing of cutlery cannot transmit Zika virus from an infected person to others.

Mosquito bites are the major source of most Zika virus infections in people. After infection, the Zika virus is present in blood and saliva for two weeks, but it remains in bodily fluids like breast milk for weeks and semen for months.

The viral loads in the saliva are very low, anti-microbial components in the saliva also making that low level of virus less infectious than it might be in another bodily fluid like blood and semen.

Saliva is a viscous liquid, that prevents the ability of the virus to move and get to cells that they could infect.
Presently, there is no cure for Zika virus
infected person should rest, stay hydrated, use painkiller drugs and avoid mosquito bites.
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Malaria drug protects fetuses from Zika

Zika virus infection can cause brain damage and sometimes death of fetus in the womb, it infects the fetus by manipulating the normal barrier to infection in the body.

Exposure to zika virus activated genes related to autophagy, the virus multiply in the placenta, autophagy process in the placenta promotes zika's survival and it infects the placental cells.

The malaria drug, Hydroxychloroquine suppresses the autophagy response, this reduces the virus in the fetuses and placentas.
With this suppression, their is less damage and the fetuses grow normally.

The malaria drug protects the fetus from the zika virus even when the virus is still present in the mother. It effectively blocks viral transmission to the fetus by interfering with the process of zika virus infection transmission and protects fetus from viral infection.

Hydroxychloroquine suppresses the autophagy response, this reduces the virus in the fetuses and placentas.
With this suppression their is less damage and the fetuses grow normally.
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Female mosquitoes transmit Zika virus to their eggs

Zika virus has been found to cause a form of brain damage- microcephaly in newborns whose mothers were infected during pregnancy.

Researchers injected laboratory-reared A. aegypti with Zika virus. The mosquitoes were fed, and they started laying eggs after some days.

 The researchers collected and incubated the eggs and reared the hatched larvae to adult mosquitoes.

They discovered that the mosquitoes passed viruses on to their offspring, including dengue fever, yellow fever and zika virus.

Keep your environment clean, destroy mosquitoes' eggs to prevent mosquitoes from breeding and spreading of Zika virus.

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How to detect Zika virus from semen samples

A reliable clinical assay that can detect the Zika virus from semen samples has been discovered by scientist. This assay can reduce Zika infection rates and allow couples who are at risk to plan their pregnancy

A total of 100 semen samples were spiked with a recombinant Accuplex ZIKV (SeraCare Life Sciences) at 5 viral copies per ml and processed in Aptima Urine Transport medium (Hologic Inc.) and tested using Aptima® ZIKV assay released under the FDA's emergency use authorization on the fully automated Panther system from Hologic, Inc.

The samples were also tested for West Nile Virus, Chagas and Dengue, recombinant Dengue Virus, recombinant Chikungunya Virus, Human Papilloma Virus, Herpes Simplex Virus 1, Herpes Simplex Virus 2, Chlamydia, and Gonorrhea.

The experiment was repeated three times and in triplicates each time.
The assay was found to be 100% sensitive and 100% specific to ZIKV RNA from semen samples with a limit of detection of 5 viral copies per mL of semen.

 Accurate diagnosis is very important for management of Zika virus and to prevent neonatal infections. Zika infection during pregnancy can cause birth defects.

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Facts about Zika virus

Zika virus is a mosquito- borne illness that is spread by the Aedes species of mosquito.

Aedes albopictus, known as the Asian tiger mosquito, and the Aedes Aegyptus, known as the yellow fever mosquito are responsible for Zika virus.

The Zika virus was first identified in monkeys, in Uganda in 1947. The first human cases were detected in Uganda and the United Republic of Tanzania in 1952.

Presently, there is no treatment for the virus. Avoiding mosquito bites is the major prevention method against Zika virus.

Signs and symptoms of Zika virus are vague and can last for up to 1 week. Diagnosis of the virus is typically confirmed with a blood test.

Major Zika virus cases occur in tropical regions, such as Brazil, Colombia, Paraguay, Suriname, Venezuela, and French Guiana.

Currently, there is no treatment for  Zika. People living with the virus must
increase their body fluid to prevent
dehydration, relieving pain and fever with acetaminophen.

 CDC advised pregnant women who are diagnosed with Zika to go for monitoring of fetal growth and anatomy program every 3-4 weeks.

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Zika virus causes more diseases in children

Zika could be more dangerous to unborn babies because test on pregnant monkeys infected with the virus found that every single fetus had picked up some trace of Zika.

 The research team infected four pregnant rhesus macaque monkeys at the Wisconsin National Primate Research Center with a Zika virus and
discovered that the virus was present in each monkey's fetus.

The research group also found damage from Zika in every part of the interface between mother and fetus - the placenta, amniotic fluid in the womb and the lining of uterus.

Three of the baby monkeys were born with small heads, but not as small as it would need to be to meet the human standard for diagnosing microcephaly.

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