Antiviral Natural Products and Herbal Medicines

Dengue has emerged as an important arboviral disease with significant impact on the disease burden in population residing in tropical countries. Dengue is spread by the bite of Aedes mosquito. The virus seems to have some hepatotoxic effects. Affliction of liver in form of derangements in the liver function tests is common and may include mild elevations in serum bilirubin, elevated transaminases and derangements in serum albumin. Although asymptomatic in most cases, clinical manifestations like jaundice, and acute liver failure (ALF) may occasionally complicate the clinical picture. Indeed, dengue has been implicated as an important cause of ALF in endemic countries. The present review focuses on the hepatic manifestations and the pathogenesis of the liver injury in dengue.

Dengue and its effects on liver.

In global health, critical challenges have arisen from infectious diseases, including the emergence and reemergence of old and new infectious diseases. Emergence and reemergence are accelerated by rapid human development, including numerous changes in demographics, populations, and the environment. This has also led to zoonoses in the changing human-animal ecosystem, which are impacted by a growing globalized society where pathogens do not recognize geopolitical borders. Within this context, neglected tropical infectious diseases have historically lacked adequate attention in international public health efforts, leading to insufficient prevention and treatment options. This subset of 17 infectious tropical diseases disproportionately impacts the world's poorest, represents a significant and underappreciated global disease burden, and is a major barrier to development efforts to alleviate poverty and improve human health. Neglected tropical diseases that are also categorized as emerging or reemerging infectious diseases are an even more serious threat and have not been adequately examined or discussed in terms of their unique risk characteristics. This review sets out to identify emerging and reemerging neglected tropical diseases and explore the policy and innovation environment that could hamper or enable control efforts. Through this examination, we hope to raise awareness and guide potential approaches to addressing this global health concern.

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Emerging and Reemerging Neglected Tropical Diseases: a Review of Key Characteristics, Risk Factors, and the Policy and Innovation Environment

Peptide entry inhibitors of enveloped viruses: the importance of interfacial hydrophobicity.

Zika virus (ZIKV) and dengue virus (DENV) are antigenically related flaviviruses that share cross-reactivity in antibody and T cell responses, and co-circulate in increasing numbers of countries. Whether pre-existing DENV immunity can cross-protect or enhance ZIKV infection during sequential infection of the same host is unknown. Here, we show that DENV-immune Ifnar1
 −/− or wild-type C57BL/6 mice infected with ZIKV have cross-reactive immunity to subsequent ZIKV infection and pathogenesis. Adoptive transfer and cell depletion studies demonstrate that DENV-immune CD8+ T cells predominantly mediate cross-protective responses to ZIKV. In contrast, passive transfer studies suggest that DENV-immune serum does not protect against ZIKV infection. Thus, CD8+ T cell immunity generated during primary DENV infection can confer protection against secondary ZIKV infection in mice. Further optimization of current DENV vaccines for T cell responses might confer cross-protection and prevent antibody-mediated enhancement of ZIKV infection. Dengue virus-specific antibody and CD8+ T cells that cross-react with Zika virus have been described. Here, the authors establish a functionally protective role for cross-reactive dengue virus-specific CD8+ T cells during challenge with Zika virus.

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Dengue virus-reactive CD8+ T cells mediate cross-protection against subsequent Zika virus challenge

Dengue viruses (DENVs) cause the most common arthropod-borne viral disease in man with 50-100 million infections per year. Because of the lack of a vaccine and antiviral drugs, the sole measure of control is limiting the Aedes mosquito vectors. DENV infection can be asymptomatic or a self-limited, acute febrile disease ranging in severity. The classical form of dengue fever (DF) is characterized by high fever, headache, stomach ache, rash, myalgia, and arthralgia. Severe dengue, dengue hemorrhagic fever (DHF), and dengue shock syndrome (DSS) are accompanied by thrombocytopenia, vascular leakage, and hypotension. DSS, which can be fatal, is characterized by systemic shock. Despite intensive research, the underlying mechanisms causing severe dengue is still not well understood partly due to the lack of appropriate animal models of infection and disease. However, even though it is clear that both viral and host factors play important roles in the course of infection, a fundamental knowledge gap still remains to be filled regarding host cell tropism, crucial host immune response mechanisms, and viral markers for virulence.

https://www.tandfonline.com/doi/pdf/10.3402/iee.v3i0.19839

Dengue viruses - an overview.

The knowledge of viral shedding patterns and viraemia in the reservoir host species is a key factor in assessing the human risk of zoonotic viruses. The shedding of hantaviruses (family Bunyavirida ...

Life-long shedding of Puumala hantavirus in wild bank voles (Myodes glareolus).

The knowledge of viral shedding patterns and viraemia in the reservoir host species is a key factor in assessing the human risk of zoonotic viruses. The shedding of hantaviruses (family Bunyaviridae) by their host rodents has widely been studied experimentally, but rarely in natural settings. Here we present the dynamics of Puumala hantavirus (PUUV) shedding and viraemia in naturally infected wild bank voles (Myodes glareolus). In a monthly capture-mark-recapture study, we analysed 18 bank voles for the presence and relative quantity of PUUV RNA in the excreta and blood from 2 months before up to 8 months after seroconversion. The proportion of animals shedding PUUV RNA in saliva, urine and faeces peaked during the first month after seroconversion, but continued throughout the study period with only a slight decline. The quantity of shed PUUV in reverse transcription quantitative PCR (RT-qPCR) positive excreta was constant over time. In blood, PUUV RNA was present for up to 7 months but both the probability of viraemia and the virus load declined with time. Our findings contradict the current view of a decline in virus shedding after the acute phase and a short viraemic period in hantavirus infection - an assumption widely adopted in current epidemiological models. We suggest the life-long shedding as a means of hantaviruses to survive over host population bottlenecks, and to disperse in fragmented habitats where local host and/or virus populations face temporary extinctions. Our results indicate that the kinetics of pathogens in wild hosts may differ considerably from those observed in laboratory settings.

Life-long shedding of Puumala hantavirus in wild bank voles

Abstract Spinal epidural hematomas (SEH) are a rare hemorrhagic event occurring after trauma, epidural anesthesia, or operative inventions. However, in 40–50% of cases, they occur spontaneously. Spontaneous spinal epidural hematomas (SSEH) are rare in occurrence with an estimated incidence of 1 case per million annually. Pregnancy is an independent risk factor. Sudden neck or back pain, often in combination with a rapid onset of neurological symptoms, is the most common presentation of SEH (1). A 36-year-old Caucasian female with rheumatoid arthritis (RA) presented to the emergency department approximately 48 h after an uncomplicated vaginal delivery. She sought medical attention due to constant headaches and neck pain that started during active labor. An MRI of the spine revealed an extensive SEH spreading from C1 to L5. The patient was without neurological symptoms or deficits and was successfully treated conservatively without any sequelae. Even though the definitive cause of this case of SEH will remain unknown, several possible synergistic mechanisms have been identified. These include female gender, full-term pregnancy, physical activity with increased intraabdominal pressure (i.e., Valsalva maneuver), systemic administration of platelet aggregation inhibitor (PAI), and iatrogenic manipulation such as spinal epidural anesthesia. Even though autoimmune and inflammatory disorders have been described in the literature to be rare sources of hemorrhage in the spinal canal, it is unclear whether the patient’s RA should be regarded as an individual risk factor. Key Facts Spinal epidural hematomas are a rare hemorrhagic event characterized by an accumulation of blood between the vertebrae and the dura of the spinal canal, and can be a clinical challenge to diagnose due to the insidious presentation, with symptoms ranging from asymptomatic to non-specific head or neck pain, or neurological deficits. The etiology of spontaneous spinal epidural hematomas remains largely unknown, although there are many predisposing factors, including vascular malformation, anticoagulation therapy, trauma, iatrogenic manipulations, and hypertension. The differential diagnosis to spinal epidural hematomas are several, e.g., meningitis, migraine, subarachnoid or intracranial hemorrhage, pituitary apoplexy, venous sinus thrombosis, and thrombosis, and radiological examination is key to diagnose and map the distribution of the hemorrhage. 

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Extensive Spinal Epidural Hematoma as the Cause of Postpartum Headache and Neck Pain After Epidural Anesthesia: a Case-Based Report

Abstract Myocarditis is an inflammatory disease of the myocardium with either focal or diffuse involvement and usually gives rise to chest pain, dyspnea, palpitations, and fatigue. In severe cases, arrythmias, syncope, and cardiogenic shock may occur. Acute myocarditis is most commonly caused by a variety of viruses with cardiotropic properties. Rare causes of myocarditis include bacterial infections. We, herein, describe a case of acute myocarditis caused by the intracellular bacterium Francisella tularensis. A young and previously healthy male in Northern Sweden was referred to the emergency department due to intense upper-chest pain and dyspnea. ECG exhibited minimal ST-segment elevations and laboratory parameters revealed pathological levels of high-sensitivity cardiac troponin and C-reactive protein. Radiological imaging showed increased metabolism in enlarged lymph nodes in the chest and signs that could be compatible with increased metabolism in the left ventricular of the heart. The combination of acute myocarditis and enlarged lymph nodes was believed to be caused by the intracellular bacterium Francisella tularensis , endemic in the Northern Sweden, and was verified with positive serology. The patient showed full recovery after antimicrobial treatment. As this is the fifth published case of myocarditis associated with Francisella tularensis, we suggest considering tularemia in acute myocarditis in tularemia-endemic area. 

/pdf/acute-myocarditis-caused-by-francisella-tularensis-a-case-vl696emm.pdf

Anne Tuiskunen Bäck

Papers

Dengue viruses - an overview.

Life-long shedding of Puumala hantavirus in wild bank voles (Myodes glareolus).

Life-long shedding of Puumala hantavirus in wild bank voles

Extensive Spinal Epidural Hematoma as the Cause of Postpartum Headache and Neck Pain After Epidural Anesthesia: a Case-Based Report

Acute Myocarditis Caused by Francisella tularensis: a Case Report