Active Ingredients: Ivermectin
What should the architecture of diagnostic research look like to provide us with an appropriate research strategy, yielding the clinical information we are looking for, with a minimum burden for study patients and an efficient use of resources?
Second, important design features for studying the accuracy and clinical impact of diagnostic tests and procedures are dealt with in more detail, addressing the cross-sectional study, the randomised trial, and the before—after study.
In addition, it is shown that the impact of diagnostic tests varies with different clinical settings and target populations, and indications are given as how to ensure that estimates of test accuracy will travel and be transferable to other settings.
Also, for clinical diagnostic studies, an overview of the most important data-analytic issues is presented, from simple two by two tables to multiple logistic regression analysis. Nowadays, for both clinical investigators and readers of research articles, it is not enough to understand the methodology of original clinical studies.
They must also know more about the techniques to summarise and synthesise results from various clinical studies on a similar topic.
Metrics details Abstract Zika virus has spread rapidly in the Americas and has caused devastation of human populations affected in these regions.
While major efforts have been undertaken to control mosquito populations that spread the virus and to develop a vaccine, drug development that directly targets the virus in an infected individual to prevent or treat the neurological manifestations is necessary.
Rational and targeted drug development is possible since the viral life cycle and the structure of the key viral proteins are now well understood.
While several groups have identified therapeutic candidates, their approaches differ in the types of screening processes and viral assays used.
Animal studies are available for only a few compounds. Here we provide an exhaustive review and compare each of the classes of drugs discovered, the methods used for drug discovery, and their potential use in humans for the prevention or treatment of neurological complications of Zika virus infection.
Introduction Zika virus ZIKV was discovered incidentally in 1947 during a yellow fever virus study in a Rhesus macaque monkey in the Zika forest of southern Uganda. Historically, human ZIKV infections remained limited to sporadic cases in equatorial Africa and Asia with only 1 small cluster of cases in Indonesia reported in 1977.
Consequently, the virus did not present a major public health concern and remained largely obscure within the medical community. In, physicians on the island of Yap in Micronesia were confronted with an epidemic form of fever, conjunctivitis, rash, and arthralgia reminiscent of dengue virus DENV infection.
Subsequently, there has been an explosion in public and scientific interest in understanding ZIKV infection and mitigating its detrimental effects.
In this review, we describe the viral life cycle in the context of therapeutic targets and describe the approaches taken for the discovery of compounds capable of preventing or treating the neurological complications associated with ZIKV infection.
The relative thermostability of the E, as compared with other flaviviruses such as DENV, is thought to contribute to the virulence of ZIKV by helping the virus survive in the unfavorable conditions of saliva, semen, and urine.
Nearly 11 kilobase pairs long, the positive-sense, single-stranded ss RNA genome encodes 3 structural and 7 nonstructural proteins.
The viral genome is encased by prM, and C, forming an immature virion. Immature virions mature when pr is cleaved from prM.
The acidic environment of the endosome induces conformational changes of the E protein, fusion of the host endosome membrane with the viral envelope, and, ultimately, the release of the RNA genome. The ssRNA is translated on the endoplasmic reticulum ER membrane into a polyprotein complex, which is cleaved by host and viral proteases in the ER lumen and cytoplasm, respectively Fig.
The mature virion attaches to the host cell membrane receptor protein, undergoes receptor-mediated endocytosis, followed by endosomal membrane-viral envelope fusion, and viral genome release into the host cytoplasm. One fixes behind the pubic binseparable to hold the condom in place, while the other ring stays outside the vagina.