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Er lumen protein1/22/2024 ![]() ![]() Subsequent clinical and pre-clinical findings further supported the causal relationship between ZIKV infection and microcephaly in newborns. The causative link between ZIKV and congenital neurological anomalies was established based on several evidence including the detection of ZIKV RNA within the amniotic fluid acquired from ZIKV-infected mothers with confirmed fetal microcephaly case. The sudden spike of microcephaly cases among newborns in Brazil following the 2015–2016 ZIKV outbreak triggered the Brazilian Ministry of Health and the World Health Organization to declare ZIKV as a national and international public health emergency. This epidemic also recorded a 20-fold increase of GBS incidence, where 41 GBS-diagnosed patients (98%) were serologically positive for ZIKV. Nevertheless, the second ZIKV outbreak in French Polynesia in 2013 provided the first compelling relationship between ZIKV infection and a neurological complication, where a woman was diagnosed with Guillain-Barré syndrome (GBS), an autoimmune disease typically affecting motor neuron functions, a week following the onset of ZIKV-like symptoms. ZIKV-infected patients typically present mild clinical symptoms such as fever, maculopapular rash, conjunctivitis, and arthralgia. The same study estimated that 5005 island residents (73%) were infected, of which 919 were symptomatic. During this outbreak, 185 suspected cases of ZIKV infection were reported, and at least 24% of these patients were either serologically or molecularly confirmed for ZIKV infection. ZIKV was put under scrutiny following its first outbreak in the Yap Island of Micronesia in 2007. Despite its discovery more than a half-century ago, ZIKV received little attention due to sporadic cases of human infection with mild and self-limiting symptoms. ZIKV was first isolated from a febrile rhesus monkey in April 1947 and was subsequently isolated from Aedes africanus mosquitoes 9 months later in Zika Forest of Uganda. Zika virus (ZIKV) is a mosquito-borne virus that belongs to the Flaviviridae family together with other notable flaviviruses such as dengue virus (DENV), West Nile virus (WNV), Japanese Encephalitis virus (JEV), and yellow fever virus (YFV). Pharmacological targeting of ZIKV-affected ER-resident proteins and ER-associated components demonstrate promising signs of combating ZIKV infection and rescuing host organisms from severe neurologic sequelae. Furthermore, the review covers several important resulting effects of ZIKV infection to the ER and cellular processes including ER stress, reticulophagy, and paraptosis-like death. This review also discusses ZIKV interaction with ER proteins such as signal peptidase complex subunit 1 (SPCS1), ER membrane complex (EMC) subunits, and ER translocon for viral replication. This review highlights the subcellular localization of ZIKV to the ER and ZIKV modulation on the architecture of the ER. Endoplasmic reticulum (ER) and ER-related proteins are essential in ZIKV genome replication. A series of outbreaks accompanied by unexpected severe clinical complications have captured medical attention to further characterize the clinical features of congenital ZIKV syndrome and its underlying pathophysiological mechanisms. It is an arbovirus that can cause congenital abnormalities and is sexually transmissible. Zika virus (ZIKV) belongs to the Flavivirus genus of the Flaviviridae family. ![]()
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