hantavirus vector art

  • 19 min read
  • Feb 23, 2020

1000+ Hantavirus Stock Images, Photos & Vectors | Shutterstock
1000+ Hantavirus Stock Images, Photos & Vectors | Shutterstock

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In 1978, the etiological agent Hemerologic Korean fever isolated from infected small field near the river rodent Apodemus agrarius Hantan in South Korea. A virus called as Hantaan virus, after the name of the river Hantan. It dates back to the early discovery of a scientific approach that began after the Korean War (1951-1953), where more than 3,000 cases of dengue fever were reported in Korea between UN forces. In 1981, Hantaan 76-118 virus strain, isolated from Apodemus agrarius grown in A549 cell line, and electron microscopic images revealed that the virus was a new member of the family Bunyaviridae. Hantaviruses observed that unlike other members of this family have arthropod vectors, and exclusively establish persistent infections in a population of rodents host their specialty. In 1981, a new genus called “hantavirus” was introduced in the family Bunyaviridae, including the virus that causes fever hemoroligic with renal syndrome (HFRS) (). It was initially thought that pathogenic hantaviruses restricted to old words. Until 1993, the only original hantavirus found in the new word is non-pathogenic virus Prospect Hill (PHV). This myth ended after the outbreak of hantavirus in the four corners of the Southwestern United States that cause serious respiratory problems in patients who are infected and led to the discovery of new hantavirus disease called hantavirus cardiopulmonary syndrome (HPS). Examination of the samples kept frozen lung tissue from people who had died of a lung disease that can not be explained in the past revealed that HPS is an old disease with a similar case dating to at least 1959. In a very short time the virus that causes HPS general affection isolated from mice (Peromyscus maniculatus,) and then called Sin Nombre virus (SNV). Later, it became clear that other hantaviruses similar to SNV, such as the Andes virus (ANDV), which is present in the united states. Currently, Hantavirus genus includes more than twenty-one species and more than 30 genotypes ().

Left panel shows the classification of negative stranded RNA virus in two groups, Mononegavirales and segmented negative stranded RNA viruses. Mononegavirales have one copy of the negative sense RNA genome and RNA viruses have multiple copies of a segmented negative sense RNA genome. segmented RNA viruses have been further classified into three families, Orthomyxoviridae, Bunyaviridae and Arenaviridae. The virus in the Bunyaviridae family have been classified into five genera, bunyavirus, Hantavirus, Nairovirus, Phlebovirus and Tospovirus. the right panel shows the reservoir of mice for hantaviruses. (A) Apodemus agrarius (Reservoir for Hantaan viruses that cause HFRS); (B) deer (Peromyscus maniculatus), (C) The Cotton Rat (Sigmodon hispidus); (D) The Rice Rat (Oryzomys palustris); (E) The White-footed mouse (Peromyscus leucopus). Rodents in B, C, D and E cause HPS. All the pictures in the right panel obtained from the CDC website;

Members of the genus Hantavirus, family Bunyaviridae

Note: The contents of the table is from reference (,)

Hantaviruses have coevolved for millions of years with rodents them and insectivore reservoir. Rodent reservoirs include rodents Cricetidae (subfamilies Arvicolinae, Neotominae and Sigmodontinae) and rats (subfamily Murinae). Cricetidae mice include mice, lemmings from the northern hemisphere and New World rats and mice. Rats include Old World rats and mice (). Hantavirus phylogeny follows closely that of their rodent hosts, showing long-term co-evolution, although there is evidence host switch occasionally in the past. The phylogenetic tree shows that the co-speciation hantavirus with their host animals from four different parts of rodents appear to affect their ability to cause a specific clinical manifestations in humans. For example, the majority of virus in Neotominae and Sigmodontinae subfamilies are known to cause severe HPS with high mortality rates (40-50%). This virus is distributed throughout North and South America on a different rodent species of New World Neotominae and Sigmodontinae rodents. Old hantaviruses world that has co-evolved with rodent Murinae causes severe HFRS which mainly affect kidney function with 0-15% mortality. Although the disease caused by a virus Murinae has less r deatheat, still poses a significant threat to human health because of the severity of the disease and the virus’ ability to cause large-scale outbreaks. Among hataviruses Arvicolinae-borne, only Puumala virus (PUUV) causes a milder form of the human disease is often referred to as epidemia nephropathi with a mortality rate of less than 1%. Interestingly, most of the other members of this subfamily are non-pathogenic to humans. Until now, the only exceptions that do not have a connection rodent confirmed is Thottapalayam virus (TPMV), which is isolated from a shrew the Asian or shrew (Suncus murinus) was arrested in 1964 during a survey for the virus Japanese encephalitis in southern India ( ).

phylogenies of hantaviruses carried by different rodent (rat family, subfamily Murinae and Family Cricetidae, subfamily Arvicolinae, Sigmodontinae and Neotominae) and insects. This tree is based on the complete coding region of segment S. HTNV, Hantaan virus; SEOV, Seoul virus; DOBV, Dobrava virus; SAAV, Saaremaa virus; PUUV, Puumala virus, TULV, Tula virus; PHV, Prospect Hill virus; BLLV, Blood virus Land Lake; ISLAV, Isla Vista virus; KHAV, Khabarovsk virus; TOPV, Topografov virus; SNV, Sin Nombre virus; NYV, viral New York; MGLV, Monongahela virus; ELMCV, El Moro Canyon virus; RIOSV, virus Rio Segundo; MULV, Muleshoe virus; BAYO, Bayou virus; BCCV, Black Creek Canal virus; LANV, Laguna Negra virus; RIOMV, Rio Mamore virus; ANDV, Andes virus; TPMV, Thottapalayam virus. In the picture, the viruses that cause HFRS is in red type and they cause HCP in blue type. The virus is not associated with disease in black type. This image obtained from the reference ()

electron microscope rejoice that hantaviruses are round or oval particles with a diameter of 80-210 nm (). They have a tripartite negative sense RNA genome (,). Large (L) genomic RNA segments encoding the RNA virus RNA dependent polymerase (RDR), size medium (M) segment encodes the viral glycoprotein precursor (GPC) which is then cleaved into two glycoproteins G1 and G2, and small (S) segment encodes the nucleocapsid protein virus (N). The nucleotide sequences at the 5 ‘and 3’ termini of each segment of the genome are complementary and experience base pair to form the panhandle structure (). In the three viral particle complex genomic RNA with N protein and nucleocapsid formed three individuals, who together with the RdRp encapsulated in a lipid envelope. Two glycoproteins G1 and G2 remain embedded in the lipid envelope ().

(a) Hantaviral sense RNA genome consists of three negative, S segment encodes the nucleocapsid protein (N), M segment encodes a glycoprotein G1 and G2, and L segment encodes the viral RdRp. structure (b) Panhandle hantaviral three RNA genome formed by the base complementary base pairing at the 5 ‘and 3’ ends of each segment of the genome. (C) Pictorial representation of hantavirus particles, showing the three nucleocapsid enveloped in a lipid bilayer. (D) Thin-section electron micrograph of the Sin Nombre virus isolates, the causative agent of Hantavirus pulmonary syndrome (HPS). (E) Pictorial representation of the life cycle of hantavirus.

Like many other viruses, hantaviruses enter host cells by the interaction between the virus and the cell surface glycoprotein integrin receptor (). Interestingly, pathogenic and non pathogenic hantavirus using different integrin receptors to enter their host cells. αIIaβ3 human integrin expressed by platelets, and αvβ3 expressed by endothelial cells mediating cellular influx of HFRS and HCP causing hantaviruses (). In contrast, non pathogenic hantaviruses, such as, PHV and TULV use of α5β1 receptor to enter the cell. Having been involved in the surface of the host cell, hantaviruses entry into cells by clathrin dependent endocytosis. After internalization, three nucleocapsid is released into the cytoplasm of the cell with the virus RdRp. Furthermore, the RdRp initiate viral transcription and mRNA encoding the three viral proteins are synthesized. viral mRNA is about 100 nucleotides shorter than their parents viral RNA genome, and the lack of a poly A tail. Viral RdRp using a novel “cap snatching” mechanism for transcription initiation. During the cap snatching 10-14 nucleotides long 5 ‘capped oligonucleotide is cleaved from the transcript of the host cell and is used as a primer by viral RdRp to initiate viral mRNA synthesis, the mechanism of prime-and-realign (,). viral mRNAs are translated in the cytoplasm of the cell by the host cell translation the machine. Viral RdRp also replicating the genome through the synthesis of complementary Crna. cRNAs complementary exact complement of the viral RNA genome (vRNA), and serves as a template for the synthesis of viral genomic negative sense. Viral assembly and maturation take place either on the cell surface or in the Golgi. Virions are due at the Golgi are transported to the cell surface via vesicular secretory pathway. In the end, new virions bud from the host cell plasma membrane.

hantavirus N protein is most abundant protein in the cytoplasm of infected cells. transcripts were detected in infected cells six hours after infection. N protein responsible for encapsidation and packaging of the viral genome. However, recent studies have shown that N is a multifunctional protein involved in viral diverse functions, including its role in the initiation of transcription and translation of viral mRNA (,). Trimeric N also recognizes vRNA panhandle with the specificity and the possibility of facilitating the incorporation of selective RNA viral genome into virions. N also been found to interact with some host cell proteins and the nature of these interactions are still unclear.

Glycoprotein precursor (GPC) is synthesized on ribosomes associated with the endoplasmic reticulum (ER) and translocation into the ER lumen by endogenous signal peptide. In the ER, GPC is post translationally cleaved in WAASA sites preserved, and two glycoproteins G1 and G2 is generated which is then glycosylation and translocation to the Golgi. Facilitating the attachment of the virion glycoprotein integrin receptor located on the surface of host cells.

Hnatavirus RdRp is a large protein with a molecular weight of 250-280 KD. Because RdRp large molecular weight is difficult to express in bacteria, and thus remains the most uncharacterized proteins in hantaviruses. RdRp mediate between transcripn and replication of the viral genome. During the RdRp synthesizes viral mRNA transcription of negative sense vRNA template. During replication replicates RdRp Crna vRNA genome through the middle. So there is a possibility that the hantavirus RdRp has several activities, including endonucleases, replicase, transcriptase and RNA helix unwinding activities. However, recent studies have shown that the virus RdRp require N protein to function. For example, a short primer capped mRNAs produced from the host cell with the process used by the cap grabbing RdRp to initiate transcription. Hnatavirus N protein has been found to be involved in the primary generation of restricted ().

The geographical distribution of hantavirus host a mirror that hantavirus epidemiology and geographical distribution (). hantavirus infection to humans is considered spill over infections that cause two types of serious illness, HFRS and HPS. The main root of infection for the two diseases are inhaling live virus through the lungs. In humans generally get hantavirus infection through direct contact with infected rodents or their droppings aerosol; although there are reports documenting the spread of the virus Andes (ANDV) from human to human (,). HFRS is caused by hantaviruses old world and most of the cases were found in East Asia (China, Korea and eastern Russia) and Europe, including the European part of Russia). Every year more than 100,000 reported cases of HFRS in China alone (), and more than 900 cases were reported in Korea and Eastern Russia (). In Europe most cases of HFRS registered in Russia, Finland and Sweden (,). Most of HFRS patients were male with ages 20 to 50 years. HFRS mortality rate depending on the type of virus and in general vary from 0.1 to 10%. HRFS patients mostly belonging to the rural areas where rodent hosts thick hantaviral inhabited. The only hantavirus that cause diseases in urban areas is Seoul virus (SEOV) because the host is the domestic rat (Rattus norvegicus and Rattus rattus). HPS has a mortality rate of 40-50% and is caused by a new world hantaviruses, including SNV, ANDV, Monongahela virus, New York virus, Black Creek Canal virus, Bayou virus, Oran virus and many other newly identified strains. Although HPS is found throughout the united states, most cases were registered in the western region and caused by the SNV. Even SNV is a species of virus are mainly found that cause HPS in patients. HPS out break in North America related to the increasing population of the host mouse deer (peromyscus maniculatus). HPS has alsoreported in other countries in South and Central America, including Argentina, Brazil, Chile, Bolivia, Paraguay, Uruguay and Panama.

World distributation different species of hantavirus

It is not exactly clear how the spread hantaviruses human body after inhalation through the lungs. However, the cells are immature dendritic (DC) may play an important role in their dissemination. Mature DC express β3 integrins, receptors that hantaviruses are used for attachment and entry. In the airways and alveoli of the lungs, DC is located around epithelial cells serves as a prime target for pathogens pick. Hantaviruses infect both adult and mature DC, which may serve as a vehicle for the transport of virions through the lymphatic vessels to regional lymph nodes, where they get a chance to infect other immune cells, such as macrophages and monocytes. After further replication or cell bound-free virions can infect endothelial cells, the main target for the virus that causes fever hemorologic ().

Increased permeability of blood vessels and decrease in platelets are the hallmarks of hantavirus-related diseases, and the pathogenic mechanisms are poorly understood. Unlike other hemorologic fever viruses such as Ebola virus, hantaviruses that do not increase the permeability of endothelial cell monolayers in vitro, also did not cause cytopathic effect on host endothelial cells. It points to the role of the host immune system in the pathogenesis of hantavirus.

Attack virus is detected early during infection by non immune cells and DC is located in the host interface pathogens (). pathogen recognition receptors (PRRS) for the detection of viruses in the host cell including TLRs and RIG-I like helicase (RIG-I and MDA5). RIG-I detects the virus from several families, including Orthomyxoviridae, Paramyxoviridae, Rhabdoviridae and Flaviviridae. However, PRRS which hantaviruses sense in the host cell still to be identified. Type I INF and other pro-inflammatory response triggered by PRR signaling induce host resistance to viral infection and activation of the innate immune cells, such as natural killer (NK) cells or NKT cells for host defense. These initial responses aimed at reducing the spread of the virus during the lag phase before the adaptive immune response is ready to attack. It is well established that treatment of cells with type I INF induces the expression of several hundred genes stimulate INF (ISGs), including MxA protein also indicated that antiviral activity against viruses of the family Bunyaviridae (,). Interestingly, most of hantaviruses pathogens have evolved strategies to sabotage the INF induced host defense mechanisms. For example, pathogenic hantaviruses (HTNV, NYV) delayed-type I INF response, including MxA expression in endothelial cells. These viruses are programmed delay in the formation of antiviral state in the host cell produces a window of opportunity for rapid replication and spread of pathogenic hantaviruses through the endothelial cell layer.

inflammatory cytokines / chemokines produced by the innate antiviral immune response represents a double-edged sword. On the one hand, they play a role in virus elimination, but on the other hand, if it is not set up correctly they can facilitate the related viral diseases. For example, TNFa can clear the virus from the infected cells with out causing cell lysis. However, at the same time TNFa can modulate endothelial barrier function by promoting blood vessel leakage by increasing leukocyte adhesion and transendothelial migration (). TNF and other cytokines thought to play a role in Ebola virus (EBOV) mediated septic shock during EBOV hemerologic fever. Although hantavirus infection in vitro DC to generate a large amount of TNFa, which is consistent with increased plasma levels of these cytokines in hantavirus-infected patients during the acute phase of HFRS. However, there is no evidence such as innate immune responses are harmful, produce “cytokine storm” is similar to the 1918 strain of influenza virus, which can contribute to the immunopathogenesis hantavirus.

In general, DC are prime targets for the virus to evade the immune system. For example, human cytomegalovirus and herpes simplex virus (viral DNA) interfere with the function of DC and induce their apoptosis by different mechanisms (). Filoviruses, such as, EBOV and mature DC Marburgvirus infect humans and hamper their transition to antigen presenting cellsand also damaging their ability to generate T-cell cytokine stimulation (). On the other hand, hantaviruses infect and activate mature DC maturation and transition them to antigen presenting cells without causing cytopathic effects. Mature DC after hantavirus infection has increased the capacity of T-cell stimulation, explains the elicitation of a strong T cell responses with long-lasting memory in patients during the acute phase of hantavirus infection (). Although the third epitope is defined for hantavirus protein, N protein is the major viral target antigen recognized by T cells, possibly because of the comparatively higher in the infected cells. In recent years the concept that the CTL response directed against hantavirus-infected endothelial cells mediates increased capillary permeability is getting more and more support from some indirect evidence. For example, T cells attract the chemokine CCL5 and CXCL10 is secreted by the endothelial cells of human lung microvascular after infection by either HTNV or SNV in vitro (). Specific hantavirus CTLs efficiently lyse human endothelial cells leading to increased vascular permeability (). Additionally, PUUV infected patients showed CTL response peaks at the onset of the disease with increased serum levels of perforin, granzyme B, and epithelial cell apoptosis marker caspase-cleaved cytokeratin-18 (,). CD8 + T cell count in patients infected PUUV greatly increased during the acute phase of HFRS, and left the long-lived memory CTL strongly to protein PUUV N (). It is entirely possible that a strong primary response is unusual long-life accounts for specific memory CTL hantavirus it. This observation indicates that the strength of antiviral CTL response and CTL target amount available in the endothelial cell layer can determine the severity of vascular damage in hantavirus-infected patients. An interesting question how the rat escape from the reservoir host blood vessel damage during remnants of persistent hantavirus infection to be answered. However, recent studies have shown that regulatory T cells may play an important role in limiting immunopathology in the natural reservoir host, but this response could interfere with viral clearance. It is hypothesized that the human immune mechanisms that downregulate response of hantavirus-specific CTL and facilitate eradication of the virus by way of non-cytolytic missing, leading to a storm CTL for elimination are faster than the virus at the expense of costly damage to the barrier of endothelial causing capillary leak fatal , Instead, the rodent hosts increased regulatory T cell responses that control the activity of CTL, which leads to the persistence of the virus without immunopathology (). The quality of the T cell response is triggered against hantaviruses determined by the DC, which is programmed via the PRRS during the early stages of infection. Thus, further investigation is needed to identify which detects PRRS hantaviruses in rat and human hosts. It is probable that the PRRS to hantaviruses in humans and rodents are different and different DC program that leads to fatal disease in humans and persistence of virus in rodent hosts. Similar to cellular immunity, hantaviruses stable and durable induce humoral immune response involving antibodies of all Ig subclasses (IgA, IgM, IgG). Antibodies against the N protein appears soon after the onset of disease and antibodies to the G1 and G2 emerge later during the progression of the disease. High antibody titers have been found in individuals who have experienced HCP years ago. Humans infected with PUUV indicate the presence of antibodies in the blood of several decades of post infection, indicating that the previously-infected individual will live long protected from infection. Tables and summarizes the immune response in humans and rodents by hantavirus infection.

Working hypothesis differential regulation of the immune response specific hantavirus reservoir host mice and humans. During their meeting with the virus DC integrate different signals received through multiple PRRS (PRR 1, PRR 2, PRR3, etc.) which determine the quality of the T-cell response to the next. (A) In the rodent reservoir host their associated hantavirus can PRR signaling DC program to stimulate Treg cells that can suppress the virus-specific CTL, which led to the persistence of the virus and at the same time prevent virus-induced immunopathology. (B) In humans, which is not adjusted to hantaviruses, PRR signaling in DC produce antiviral dominant CTL response. As a result, hantavirus infected endothelial cells (EC) removed immediately lead to immunopathology

Note :. This image was obtained from Ref ()

Summary of immune response in humans for hantavirus infection

Note: The contents of this table is from reference ()

Summary of immune response in rodents during infection hantavirus

Note: the contents of this table is from reference ()

As described by the centers for Disease Control and Prevention (CDC), patients with HCP usually presents febrile prodrome A short 3-5 day (). In addition to fever and myalgia, early symptoms include headache, chills, headache, non-productive cough, nausea, vomiting and other gastrointestinal symptoms. Malaise, diarrhea, and dizziness were reported by about half of all patients, with reports of less frequent arthralgia, back pain, and abdominal pain. Patients may report breathlessness (respiratory rate normally 26-30 breaths per minute). Typical findings at initial presentation include fever, tachypnea and tachycardia, the physical examination is usually normal.

Analysis of clinical, laboratory, and data autopsy of seventeen patients with hantavirus infection was confirmed during the 1993 outbreak of hantavirus rejoiced, the mean duration of symptoms prior to hospitalization was 5.4 days. The most common symptoms at the time of hospitalization are fever, myalgia, headache, cough, and nausea or vomiting (Table and), with myalgia be early symptoms most frequently reported. The most common physical findings are tachypnea and tachycardia (TablesTables and). Fifty percent of patients had a respiratory rate of 28 breaths per minute or more, and 50 percent had a heart rate of 120 or more beats per minute. None of the patients had conjunctival hemorrhage, petechial rash, clinical signs of internal bleeding (including positive guaiac fecal specimens) or peripheral edema or periorbital. The findings of hematology famous including a white-cell count increases with an increase in neutrophils, a precursor of myeloid, and atypical lymphocytes

The symptoms in 17 patients with hantavirus infection

Note: The contents of this table is from reference ( )

the symptoms in 10 pediatric patients (aged ≤16 years) with SNV infection

Note: the contents of this table is from reference ()

clinical findings on when you sign in 17 patients with hantavirus infection

Note: The contents of this table is from reference ()

clinical findings on admission in nine pediatric patients with SNV infection.

Resoiratory level> 25 breats / min (aged 10-13 years). respiratory rate> 20 breaths / min (aged ≥14 years). Including 2 patients were mechanically ventilated before entering

Note :. The contents of this table is from reference ()

partial-thromboplastin time of 40 seconds or more in 67 percent of patients at the time of admission (TablesTables and). Despite minimal abnormalities of renal function are common, serum creatinine levels did not rise above 2.5 mg per deciliter (220 umol per liter) in patients (Tables and). The mean weight of the urine at the time of admission was 1.024 ± 0.010. Forty percent of patients had proteinuria at the entrance. dipstick urine test positive in the blood of fifty-seven percent of the patients who were tested on admission

The results of laboratory studies during hospitalization in patients with hantavirus infection

Note :. The contents of this table is from reference ()

The results of laboratory studies on admission in pediatric patients with Sin Nombre hantavirus infection

Note :. The contents of this table is from reference ()

chest radiograph early showed interstitial or interstitial and alveolar infiltrates () in sixty-five percent, infiltrate the alveolar hairy at twelve percent, and no abnormalities within twenty-four percent of patients. Furthermore, ninety-four percent has grown rapidly, bilateral diffuse infiltrates, and six percent had interstitial infiltrates limited to the lower lobe. pleural effusion noted during the course of the disease in four patients. Eleven of the twelve patients (ninety two percent) who underwent chest radiography and measurement of arterial oxygen saturation at the time of acceptance have both pulmonary infiltrates or arterial oxygen saturation below 90 mm Hg. Similar observations werhantavirus-infected e made in other cases (,)

Radiography shows the evolution of hantavirus pulmonary syndrome in women 30 years. (A) Chest X-rays before the onset of the disease. (B) radiographs of Registration. (C) radiographs after intubation. (D) radiographs prior to death

Note :. This image was obtained from Ref ()

Since the emergence of the HCP in the United States in 1993, only 5.5% of the cases reported to the CDC were children less than sixteen years. Because the minimum causality in young children and adolescents, the hypothesis that hantavirus infection in children less likely to develop into a serious illness than adults. Analysis of clinical data of pediatric SNV ten cases presented in Table -.

Hnatavirus infection was diagnosed on the basis of a positive serological test and confirmation of viral antigens in patients infected tissue or the presence of viral RNA sequences in a patient’s blood or tissue, together with a compatible history of the disease.

During the 1993 hantavirus outbreak, cross-reactive antibodies to hantaviruses previously known, such as, Hantaan, Seoul, Puumala and Prospect Hill virus found in acute- and healing-phase sera of some patients with HPS. Since then, tests based on viral antigen from SNV has been developed and is widely used for routine diagnosis of HPS. Enzyme-linked immunosorbent assay (ELISA) is a popular test for the detection of IgM antibodies in the blood of patients being brought against Hantaviruses during infection.

An IgG test in conjunction with IgM-capture test is also used for the diagnosis of hantavirus disease. Acute and recovery-phase sera should reflect the four-fold rise in antibody titer presenc IgG or IgM in the acute phase sera positive for hantavirus infection. It may be noted that the acute phase serum is used as an early diagnostic specimens may not have IgG. IgG antibodies are durable, sustained for many years after infection. Accordingly, SNV IgG ELISA has been used in the investigation of serological epidemiology of the disease and it seems appropriate for this purpose. Rapid immunoblot test strips (RIBA) is the prototype assay was studied for identification of serum antibodies specific recombinant proteins and peptides for SNV and other hantaviruses. Also, neutralize plaque test was recently conducted for serological confirmation SNV infection. However, this particular test is not commercially available. Hantaviruses isolation from human sources is difficult and there is no SNV-like virus isolates have been recovered from humans. Thus, hantavirus isolation is not considered for diagnostic purposes.

IHC testing formalin-fixed tissue with specific monoclonal and polyclonal antibodies can be used to detect hantavirus antigens and has proven to be a sensitive method for laboratory confirmation of infection hantaviral. IHC has an important role in the diagnosis of HPS in patients from whom serum samples and frozen tissue is not available for diagnostic testing and in a retrospective assessment of the prevalence of the disease in the defined geographical area.

reverse transcriptase polymerase chain reaction (RT-PCR) is a highly sensitive assay can be used to detect RNA hantaviral in infected samples, such as lung tissue and blood clots from the infected patient. However, RT-PCR is very susceptible to cross contamination and should be considered an experimental technique with limited use for diagnostic purposes hantavirus infection.

Various Infectious etiology, such as pneumonia, sepsis, with ARDS and acute bacterial endocarditis can often be confused with HPS. Other conditions commonly found in the southwestern United States have a presentation similar to HPS, such as septicemic plague, tularemia, histoplasmosis, and coccidioidomycosis. In addition, non-infectious conditions, including myocardial infarction and pulmonary edema Goodpasture syndrome should also be considered.

Apart from supportive care is no treatment for hantavirus infection at this time. Patients received broad-spectrum antibiotics while awaiting the results of laboratory diagnostic tests to confirm hantavirus-related diseases. early supportive care including the use of antipyretics and analgesics. Patient immediately transferred to an intensive care unit (ICU) if the initial symptoms showed high probability of HPS. ICU management should include careful assessment, monitoring and adjustment of volume status and cardiac function, including inotropic and vasopressor support if necessary. Fluids should be administered with caution because of the possibility of higher than capillary leakage. supplemental oxygen is required for patients with hypoxia. Due to the high risk of respiratory failure, ICU management must maintain the equipment and materials for intubation and mechanical ventilation are available. HPS patients with severe rapidly progressing to respiratory failure, and absence of ECMO (extracorporeal membrane oxygenation) nearly all patients die within 24-48 hours of the onset of this severe phase.

Antiviral therapy included the use of ribavirin, guanosine analog, has not been proven effective for the treatment of HPS. However, efficacy trials in patients with HFRS in China have demonstrated a significant beneficial effect of ribavirin if started in the early course of the disease. Although ribovarin perturbs SNV replication in vitro, not an open-label trial conducted during the outbreak in 1993 or trial showed clinical benefit sought placebo for HPS. However, it has been suggested that ribavirin efficacy may depend on the phase of infection and severity of disease at the time of administration. Ribavirin is not recommended for the treatment of HPS and is not available for this use.

Examination neutralizing antibody titers in patients on admission revealed a low antibody titers in patients with severe disease and higher antibody titers in patients with mild disease. These observations provide guidance on the use of human neutralizing antibodies during the acute phase of HPS that may prove effective for the treatment and / or prevention of infection hantaviral.

There is no FDA-approved vaccine for hantavirus infection in the UNITED STATES. Killed virus vaccine against hantavirus infection have been developed in Korea and China. However, such approaches are not persuaded in the USA for various reasons. Efforts are underway to develop a DNA vaccine, based gene rubber approach to the transport of expression plasmids containing the gene segment of M for the individual, the expression will produce antibodies against the glycoprotein G1 and G2.

high titers of antibodies have been found in individuals who have experienced HPS years ago (,). Neutralizing antibody against PUUV have been detected in individuals decades after infection (). These observations indicate that an infected person previously protected for life from reinfection. There are no known re-infection with homologous hantavirus. Closely related hantaviruses, such as Seoul and Hantaan virus, seems to cross-protect against re-infection in experimental animals, and one might expect cross-protection between hantaviruses comes from the rodent sigmodontine.

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Grunge Textured HANTAVIRUS Stamp Seal With Ribbon Stock Vector …

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Yosemite deer mice being trapped, killed following virus outbreak …

Hantavirus Vector Rat Transparent & PNG Clipart Free Download - YWD
Hantavirus Vector Rat Transparent & PNG Clipart Free Download – YWD

Hantavirus
Hantavirus

Hantavirus Detections in San Diego County
Hantavirus Detections in San Diego County

Hantavirus Vector Images (21)
Hantavirus Vector Images (21)

County Vector Control Finds Mouse in Julian Infected with Deadily ...
County Vector Control Finds Mouse in Julian Infected with Deadily …

Scratched textured hantavirus stamp seal. Hantavirus seal print ...
Scratched textured hantavirus stamp seal. Hantavirus seal print …

Hantavirus Vector Deer Mice Transparent & PNG Clipart Free ...
Hantavirus Vector Deer Mice Transparent & PNG Clipart Free …

Grunge HANTAVIRUS Scratched Round Watermarks Stock Vector ...
Grunge HANTAVIRUS Scratched Round Watermarks Stock Vector …

1000+ Hantavirus Stock Images, Photos & Vectors | Shutterstock
1000+ Hantavirus Stock Images, Photos & Vectors | Shutterstock

Hantavirus Reminder Issued After Two Deer Mice Test Positive ...
Hantavirus Reminder Issued After Two Deer Mice Test Positive …

Blue Stripe with HANTAVIRUS Text Clip Art | k66049189 | Fotosearch
Blue Stripe with HANTAVIRUS Text Clip Art | k66049189 | Fotosearch

Hantavirus Infection | American Society of Nephrology
Hantavirus Infection | American Society of Nephrology

Hantavirus Text Rubber Seal Stamp Watermark With Bonus Christmas ...
Hantavirus Text Rubber Seal Stamp Watermark With Bonus Christmas …

Yearly number of hantavirus cases in Belgium as diagnosed by the ...
Yearly number of hantavirus cases in Belgium as diagnosed by the …

Global geographic distribution of hantavirus pulmonary syndrome ...
Global geographic distribution of hantavirus pulmonary syndrome …

Hantavirus Vector Virus Transparent & PNG Clipart Free Download - YWD
Hantavirus Vector Virus Transparent & PNG Clipart Free Download – YWD

Hantavirus Stock Photos & Hantavirus Stock Images - Alamy
Hantavirus Stock Photos & Hantavirus Stock Images – Alamy

Hantavirus Vector Images (21)
Hantavirus Vector Images (21)

Of Mice, Men, and Microbes: Hantavirus: David R. Harper, Andrea S ...
Of Mice, Men, and Microbes: Hantavirus: David R. Harper, Andrea S …

Hantavirus entry: Perspectives and recent advances - ScienceDirect
Hantavirus entry: Perspectives and recent advances – ScienceDirect

Deer Mouse with Potentially Deadly Hantavirus Found in Fallbrook ...
Deer Mouse with Potentially Deadly Hantavirus Found in Fallbrook …

Hantavirus Artwork High-Res Vector Graphic - Getty Images
Hantavirus Artwork High-Res Vector Graphic – Getty Images

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