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"Dengue is the leading mosquito-borne viral illness infecting humans !"
Dengue is caused by infection with any of the four dengue virus serotypes. This review highlights the mechanisms underlying the clinical course of a dengue infection, which can range from mild febrile illness through to hemorrhagic fever and circulatory shock. It also outlines the epidemiology, pathogenesis, diagnosis and management of dengue infection.
Key phases of dengue infection
Dengue is a mosquito-borne disease caused by infection with dengue virus (DENV). Clinically, the disease can range from a mild febrile illness (previously called dengue fever) through to dengue with warning signs and severe dengue, which includes what were previously called dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS).
DENVs belong to the genus Flavivirus of the Flaviviridae family. The four serotypes are enveloped, spherical viral particles with a diameter of approximately 500 Å20. The genome of each serotype comprises approximately 11 kb of positive-sense, single-stranded RNA that encodes ten proteins. The three structural proteins encoded by the genome are the membrane (M) protein, envelope (E) protein and capsid (C) protein; the non-structural (NS) proteins are NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5.
"The viral receptor on human cells plays a critical role in disease progression !"
Viruses enter cells and initiate infection by binding to their cognate cell surface receptors. The expression and distribution of viral entry receptors therefore regulates their tropism, determining the tissues that are infected and thus disease pathogenesis. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the third human coronavirus known to co-opt the peptidase angiotensin-converting enzyme 2 (ACE2) for cell entry. The interaction between SARS-CoV-2 and ACE2 is critical to determining both tissue tropism and progression from early SARS-CoV-2 infection to severe coronavirus disease 2019 (COVID-19). Understanding the cellular basis of SARS-CoV-2 infection could reveal treatments that prevent the development of severe disease, and thus reduce mortality.
Key phases of disease progression
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to angiotensin-converting enzyme 2 (ACE2). Initial infection of cells in the upper respiratory tract may be asymptomatic, but these patients can still transmit the virus. For those who develop symptoms, up to 90% will have pneumonitis, caused by infection of cells in the lower respiratory tract. Some of these patients will progress to severe disease, with disruption of the epithelial-endothelial barrier, and multi-organ involvement.
As with all coronaviruses, SARS-CoV-2 cell entry is dependent on its 180-kDa spike (S) protein, which mediates two essential events: binding to ACE2 by the amino-terminal region, and fusion of viral and cellular membranes through the carboxyl-terminal region. Infection of lung cells requires host proteolytic activation of spike at a polybasic furin cleavage site. To date, this cleavage site is found in all spike proteins from clinical SARS-CoV-2 isolates, as well as some other highly pathogenic viruses (e.g., avian influenza A), but it is absent from SARS-CoV and is likely to have been acquired by recombination between coronaviruses in bats. Cleavage by the furin protease therefore expands SARS-CoV-2 cell tropism and may have facilitated transmission from bats to humans. Membrane fusion also requires cleavage by additional proteases, particularly transmembrane protease serine 2 (TMPRSS2), a host cell surface protease that cleaves spike shortly after binding ACE2. SARS-CoV-2 tropism is therefore dependent on expression of cellular proteases, as well as ACE2.
As part of your antenatal care you’ll be offered several blood tests. Some are offered to all women, and some are only offered if you might be at risk of a particular infection or inherited condition.
All the tests are done to check for anything that may cause a problem during your pregnancy or after the birth, or to check that your baby is healthy, but you don’t have to have them if you don’t want to.
Talk to your midwife or doctor and give yourself enough time to make your decision. They should also give you written information about the tests. Below is an outline of all the tests that can be offered.
A new diagnostic will allow men to bypass painful biopsies to test for aggressive prostate cancer.
Current tests such as the prostate specific antigen (PSA) and digital rectal exam (DRE) often lead to unneeded biopsies and more than 50% of men who undergo biopsy do not have prostate cancer, yet suffer the pain and side effects of the procedure such as infection or sepsis.
Less than 20% of men who receive a prostate biopsy are diagnosed with the aggressive form of prostate cancer that could most benefit from treatment. A newly developed diagnostic will allow men to bypass painful biopsies to test for aggressive prostate cancer. The test incorporates a unique nanotechnology platform to make the diagnostic using only a single drop of blood, and is significantly more accurate than current screening methods.
Immunology Cutaneous leishmaniasis is a major public health problem and causes a range of diseases from self-healing infections to chronic disfiguring disease. Currently, there is no vaccine for leishmaniasis, and drug therapy is often ineffective. Since the discovery of CD4+ T helper 1 (TH1) cells and TH2 cells 30 years ago, studies of cutaneous leishmaniasis in mice have answered basic immunological questions concerning the development and maintenance of CD4+ T cell subsets. However, new strategies for controlling the human disease have not been forthcoming. Nevertheless, advances in our knowledge of the cells that participate in protection against Leishmania infection and the cells that mediate increased pathology have highlighted new approaches for vaccine development and immunotherapy. In this Review, we discuss the early events associated with infection, the CD4+ T cells that mediate protective immunity and the pathological role that CD8+ T cells can have in cutaneous leishmaniasis.
Cutaneous leishmaniasis — which is caused by several protozoal parasites of the genus Leishmania — is endemic to South and Central America, Northern Africa, the Middle East and parts of Asia, and an estimated 1 million new cases arise each year. Of particular interest to immunologists is the wide range of clinical manifestations associated with this disease, which, similar to tuberculosis and leprosy, is dictated largely by the type and magnitude of the immune response of the host. As in most infections, the immune response to cutaneous leishmaniasis depends on many host factors, as well as on the differences between the infecting Leishmania spp. Experimental infections in mice also exhibit a spectrum of clinical presentations depending on the mouse strain and the infecting parasite species or strain used.
Cutaneous leishmaniasis exhibits a wide spectrum of clinical presentations that is determined largely by the host immune response. The host immune response to infection is influenced both by host genetics and the Leishmania spp. and/or strain.
The rapid recruitment of neutrophils and inflammatory monocytes following infection with Leishmania influences the course of disease. Neutrophils can have both protective and deleterious roles, whereas inflammatory monocytes kill Leishmania parasites and differentiate into monocyte-derived dendritic cells that promote the development of protective CD4+ T helper 1 (TH1) cells.
Control of Leishmania infection depends on the production of interferon-γ by CD4+ TH1 cells, which leads to enhanced killing by macrophages due to the production of reactive oxygen species and nitric oxide.
CD8+ T cells recruited to Leishmania lesions exhibit a cytolytic profile and lyse infected cells without killing the parasites, which leads to enhanced inflammation and increased severity of disease. Controlling these pathogenic CD8+ T cells, or the downstream mediators of inflammation that they induce, is a new approach to leishmaniasis immunotherapy.
Infection with Leishmania generates several types of CD4+ T cells that mediate resistance to reinfection, including effector T cells, effector memory T cells, central memory T cells and tissue-resident memory T cells. There is currently no Leishmania vaccine, and a hurdle for vaccine development is that the most effective T cells are short-lived effector T cells; targeting longer lived central memory and tissue-resident memory T cells is an alternative approach.
Herpes gladiatorum is an infection caused by herpes simplex virus type 1, a virus similar to that which causes cold sores. It is common among those who engage in high-contact sports, such as wrestling, and is also known as mat herpes. Those infected with herpes will carry the virus with them for life as there is no cure.
There will be periods where the virus is inactive and no symptoms are present, and times where it is active and causes various symptoms and flare-ups.
When the virus is active, the person carrying it is infectious and can spread herpes gladiatorum to others. The virus can be transmitted by skin-to-skin contact and is easily passed from one person to the next.
In this article, we examine the symptoms of herpes gladiatorum and the parts of the body that can be affected. We also take a look at diagnosis, treatment, and prevention of the condition.
Gastritis is a condition where the inner lining of the stomach gets inflamed. It is often caused by consumption of excessive alcohol and even due to usage of anti-inflammatory drugs. It is mainly caused by the bacterial infections and several autoimmune disorders can lead to gastritis.
The symptoms of gastritis are indigestion, abdominal pain, nausea, vomiting and heartburn. Taking a multivitamin supplement is highly beneficial for those people suffering with gastritis. By eating a balanced diet and reducing stress, one can treat gastritis. Vitamins and minerals which function as antioxidant are best remedies to improve the digestive health.
Essential Vitamins For Gastritis
1. Vitamin C
Vitamin C is an essential nutrient for the functioning of several metabolic reactions in animals and plants. Since it cannot be produced in the body, vitamin C must be taken from foods. Vitamin C deficiency can cause scurvy in humans.
This vitamin helps the body to absorb calcium and iron salts in the body. And they help to aggravate the digestive process and can reduce the irritation in the inner lining of the stomach. People who take vitamin C can control and cure gastritis. Vitamin C is present in a variety of foods and some of them are oranges, guavas, green peppers, parsley, broccoli and papayas.
2. Vitamin A
Vitamin A plays an important role in many functions that take place in our body. It also functions as retinoic acid, which is an essential hormone required for growth of epithelial cells. Vitamin A is required for various intrinsic processes.
It helps in promoting vision and enhances immune system functioning. Beta-carotene which is a precursor of vitamin A is an antioxidant, that can be obtained from many foods. It is recommended to take vitamin A in small doses and foods that rich in vitamin A are sweet potatoes, carrots, milk, paprika, turnips, lettuce and apricots.
3. Vitamin B6
Vitamin B6 is a water soluble vitamin, which helps in the functioning of several enzymatic reactions. It is also involved in different metabolisms and synthesis of hemoglobin. Pyridoxal phosphate is the active form of vitamin B6 to act as a co-enzyme with other enzymes that are particularly involved in metabolic activities.
Vitamin B6 is also an antioxidant, helps in controlling the levels of homocysteine and improves digestive functioning. The food sources that are having vitamin B6 are avocados, meat, nuts, poultry, whole grains, bananas and legumes.
4. Vitamin B12
Vitamin B12 is an important vitamin that functions the nervous system and helps in the formation of blood. It is a part of the B vitamins and is water soluble. Vitamin B12 is also required to make DNA and the genetic material in the cells.
Naturally vitamin B12 is bound to the proteins and only when the stomach releases hydrochloric acid, vitamin B12 gets separated. People with gastritis needs to take high doses of vitamin B12 to get absorbed properly. Foods that are rich in vitamin B12 are oysters, liver, octopus, crab, beef, cheese and fish.
5. Vitamin E
Vitamin E is a fat soluble compound required for many biological functions. It is an antioxidant which prevents accumulation of the free radicals in the tissues. It can be easily propagated into cell membranes to protect them from oxidation damage.
Vitamin E helps in soothing the stomach and periodically heals the lining of the stomach. By taking vitamin E as a part of the diet, one can reduce the inflammation and cure the gastritis. Foods that are rich in vitamin E are almonds, pine nuts, sunflower seeds, basil, apricots and peanuts.
Hepatitis C (HCV) is a viral infection that affects the liver and an estimated 3.2 million people in the USA are infected with HCV, and most do not feel ill or know that they are infected. Since 2010, acute cases of HCV have more than doubled, with new cases predominantly among young, white individuals with a history of injection drug use.
The current recommendations are that doctors screen patients at high-risk for contracting HCV, which include but are not limited to people born between 1945 and 1965, those diagnosed with HIV, children born to HCV-positive women and individuals who engage in injection drug use (PWID), among other select populations at high risk. This strategy is called "targeted" screening. "Routine" screening, as defined in the study, tests all individuals in a community with a high prevalence of HCV.
Video: One step Hepatitis C Virus Test Cassette, Raecho International
There are two ways to perform these screenings. Rapid testing is when results are given on the same day that the sample is drawn. Standard testing requires patients to return for a second appointment to get the results. Scientists at Boston Medical Center (Boston, MA, USA) and their colleagues evaluated the clinical benefits and cost-effectiveness of testing strategies among 15 to 30-year-olds at urban community health centers. They developed a decision analytic model to project quality-adjusted life years (QALYs), lifetime costs (2016 USDs) and incremental cost-effectiveness ratios (ICER) associated with nine strategies for one-time testing. The strategies differed in three ways: targeted versus routine testing; rapid finger stick versus standard venipuncture; and ordered by physician versus counselor/tester using standing orders.
Illustration of the Hepatitis C Virus
The team found that compared to targeted risk-based testing (current standard of care), routine testing increased lifetime medical cost by USD 80 and discounted QALYs by 0.0013 per person. Across all strategies rapid testing provided higher QALYs at a lower cost per QALY gained, and was always preferred. Counselor-initiated routine rapid testing was associated with an ICER of USD 71,000/QALY gained. Results were sensitive to offer and result receipt rates. Counselor-initiated routine rapid testing was cost-effective (ICER greater than USD 100,000/QALY) unless the prevalence of PWID was greater than 0.59%, HCV prevalence among PWID less than 16%, reinfection rate greater than 26 cases per 100 person-years, or reflex confirmatory testing followed all reactive venipuncture diagnostics.
Sabrina A. Assoumou, MD, MPH, an infectious disease physician and lead author of the study, said, “When standard testing was applied, patients were less likely to come back for that second appointment to get their results, which in turn meant more people weren't getting the treatment they so desperately needed. Our results indicate that we must initiate rapid testing strategies so that more people will know their status and get treatment more quickly.” The study was published on September 9, 2017, in the journal Clinical Infectious Diseases.
