The Zika virus (ZIKV), an emerging mosquito-borne flavivirus that has spread like wildfire to 30 countries in the Americas. In the USA, Puerto Rico’s poor are beginning to succumb to the virus and pregnant women are transmitting the virus to the developing fetus causing a horrible brain defect called microcephaly. Harmful pregnancy outcomes include fetal brain abnormalities and microcephaly, a condition characterized by a reduction in head circumference that is often associated with delayed brain development in the fetus.
The American gulf coast is predicted to be ground zero for the virus this summer. Cities such as Houston, New Orleans and Miami are beginning to experience the rainy season with increasing heat (exacerbated by climate change) creating a favorable environment for the Aedes aegypti mosquito to replicate rapidly. Those bitten by an infected mosquito can expect illness with symptoms of fever, rash, joint pain, and conjunctivitis.
The CDC has warned that Zika is transmitted through several routes, including mosquito bites, sexual contact (heterosexual and homosexual), and blood transfusions.
In the case of pregnant women, scientists have discovered how the Zika virus can infect and replicate in immune cells from the placenta, without killing them. Results have been published 5- 27-16 in Cell Host & Microbe.
MedicalExpress reports:
"Our results substantiate the limited evidence from pathology case reports," says senior author Mehul Suthar, PhD, assistant professor of pediatrics at Emory University School of Medicine.. "It was known that the virus was getting into the placenta. But little was known about where the virus was replicating and in what cell type."
Scientists led by Suthar and pediatric infectious disease specialist Rana Chakraborty, MD found that Zika virus could infect placental macrophages, called Hofbauer cells, in cell culture. The virus could also infect another type of placental cell, called cytotrophoblasts, but only after a couple days delay and not as readily. Other researchers recently reported that syncytiotrophoblasts, a more differentiated type of placental cell than cytotrophoblasts, are resistant to Zika infection.
The cells for the experiments were derived from full-term placentae, obtained from healthy volunteers who delivered by Cesarean section. The level of viral replication varied markedly from donor to donor, which hints that some women's placentae may be more susceptible to viral infection than others.
"Not every pregnant woman who is infected by Zika transmits the virus to her fetus," Suthar says. "Host genetics and non-viral factors, including nutrition and microbiota, as well as timing may be influencing infectivity. A better understanding of these factors could allow the design of preventive measures, and eventually antiviral therapies."
From the study. ( see text for references )
The mechanism by which ZIKV crosses the placenta to establish infection in the developing fetus is not well understood. Recent studies have identified ZIKV RNA in amniotic fluid and fetal and newborn brain tissue and ZIKV-specific IgM antibodies have been detected in newborn cerebrospinal fluid. Additionally, ZIKV antigen was found in the chronic villi of a human placenta from a mother who gave birth to an infant with microcephaly, and ZIKV RNA has been isolated from placental tissue of mice infected with ZIKV. Finally, a recent study detected ZIKV antigen in placental tissue from a mother diagnosed with ZIKV disease. In particular, ZIKV antigen was detected in placental macrophages and histiocytes in the intervillous space.
Vertical transmission of ZIKV from an infected mother to the developing fetus in utero reflects tropism for placental cells. This organ is a target for a number of viruses by direct and contiguous infection of the cell layers, virion passage through a breach, or cell-associated transport. Examples include rubella, cytomegalovirus, herpes simplex, HIV-1, hepatitis B and C virus, and parvovirus B19. The placenta is characterized by contact between the maternal blood and fetal chorionic villi. Each villus is lined by trophoblasts, which encase the fetal blood supply and placental macrophages (Hofbauer cells [HCs]). Several studies have confirmed HCs are targets of viral infection in vivo and in vitro. In contrast, syncytiotrophoblasts (differentiated cytotrophoblasts [CTBs]) have been shown to be resistant to infection by a wide range of viruses. A recent study showed that syncytiotrophoblasts also appear to be resistant to infection by phylogenetically related, historic ZIKV strains at early times following infection (24 and 48 hr post-infection [hpi]).
It is important to note that, unfortunately, the GOP refuses to act on the funding request that the Centers for Disease Control and Prevention says they need to research, combat and control the Zika virus with the hope of discovering antiviral therapies. They just took yet another vacation without acting. Shame on them.
The study concludes:
These findings stress the importance of developing antiviral therapies directed against ZIKV replication within placental cells as a means to reduce vertical transmission in the mother-infant dyad and the incidence of adverse pregnancy outcomes and fetal abnormalities.
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