Hantavirus infection. hemorrhagic fever with renal syndrome (renal syndrome)

In June 1993, the recently discovered hantavirus was identified as the causative agent of an outbreak of severe respiratory illness in the southwestern United States.

The disease is now called hantavirus pulmonary syndrome. Hundreds of cases have been reported due to closely related hantaviruses. The disease is characterized by a febrile prodromal period, followed by rapid development of noncardiogenic lungs and hypotension or shock. More than 50% of patients with Hantavirus Pulmonary Syndrome have died.

Etiology

Hantaviruses are a genus belonging to the Bunyavirus family. Hantaviruses possess a supercapsid and contain an RNA minus strand made up of three unique segments. Several pathogenic viruses have been identified within the genus, including the Hantaan virus, which causes the most severe hemorrhagic fever with renal syndrome, occurring mainly on the Asian mainland; Dubrava virus; Puumala virus, Seoul virus. Prospect Hill hantavirus is widespread and spread by gray voles, but diseases caused by this virus have not been described in humans.

Cases of hantavirus pulmonary syndrome identified in 1993 were caused by Sin-Nombr virus, isolated from a deer hamster in New Mexico. Many of the causative agents of hantavirus pulmonary syndrome known to date belong to the same genetic group of hantaviruses and are associated with rodents. The habitats of these rodents are limited to the American continent, therefore, hantavirus pulmonary syndrome considered a disease of the Western Hemisphere.

Epidemiology

Usually, patients have a history of recent outdoor contact with deer hamsters or living in an area where many of these rodents live. Clustered cases of hantavirus pulmonary syndrome have been observed among workers cleaning rodent-infested homes. Approximately 50% of cases occur between May and July. Almost all patients are people from 12 to 70 years old, 60% of them are aged 20-39 years. In children under 12 years of age, cases of the disease are rare. 2 / h of patients are men, which probably reflects their more active activity in the fresh air. The reason for the almost complete absence of cases of the disease among young children - congenital immunity or lack of contact with the pathogen - is unknown. During outbreaks in Argentina, human transmission has been proven.

Hantaviruses cause lifelong asymptomatic infection in their reservoir animals. Infected animals can shed the virus in saliva, urine, and feces for many weeks, but the duration of shedding and the period of maximum infectivity remain unknown. The presence of the virus in saliva, the sensitivity of these animals to parenteral infection with hantaviruses, and field observations of infected rodents indicate that bites are an important mechanism for the spread of the virus among rodents. Infection of a person involves aerosols formed from saliva or the secretions of rodents. People who visited places of animal care, where rodents found shelter, became infected after contacts that lasted at least 5 minutes. It is possible that hantaviruses are spread through contaminated food and wounds to the skin or mucous membranes; transmission to humans occurred through rodent bites. Human-to-human transmission of hantavirus is extremely rare, but recorded in Argentina.

Symptoms

In hantavirus pulmonary syndrome, the prodromal and cardiopulmonary stages are distinguished. On average, 5.4 days pass from the onset of prodromal symptoms to hospitalization. The average duration of time from the onset of symptoms to death is 8 days (median 7 days, fluctuations range 2-16 days). In the prodromal period, the most common are fever and myalgia (100%), cough or shortness of breath (76%), gastrointestinal disorders, including vomiting, diarrhea and in the middle abdomen (76%), (71%). The cardiopulmonary stage is manifested by an increasing cough and shortness of breath. Physical examination during this period most often reveals rapid breathing (100%), tachycardia (94%) and hypotension (50%). In the most severe course, acute pulmonary edema, hypoxia and shock rapidly develop. In fatal cases, pulmonary edema was accompanied by severe hypotension, often leading to sinus bradycardia, electromechanical dissociation, ventricular tachycardia or atrial fibrillation. Arterial hypotension can worsen even with adequate treatment.

Diagnostics

Hantavirus pulmonary syndrome should be considered in a previously healthy person who developed acute respiratory failure after a period of fever. Thrombocytopenia in combination with a febrile prodromal period and contact with wild rodents in the spring or summer months indicates a high probability of hantavirus. To confirm the diagnosis, antibodies to Hantavirus class M are determined. Hantavirus antigen can be detected in tissues by immunohistochemical study or amplification of the nucleotide sequence of the Hantavirus by reverse transcription PCR. Help with diagnosis, epidemiological research and outbreak containment is available from the Department of Health.

Treatment

Adequate oxygenation must be ensured and cardiovascular function must be maintained. The pathophysiology of hantavirus pulmonary syndrome is similar to that of shock in dengue fever. For the treatment of arterial hypotension with clinical manifestations, vasopressor or inotropic agents should be used in combination with intravenous administration of reasonable volumes of fluid so as not to aggravate pulmonary edema. Ribavirin, early intravenous administration of which sometimes saves lives in hemorrhagic fever with renal syndrome, is useless in hantavirus pulmonary syndrome.

Forecast

The lethality is about 50%. Sharp deviations in hematocrit, leukocyte count, LDH and APTT are highly specific and sensitive predictors of death.

Prevention

The only way to prevent hantavirus infection is to avoid contact with rodents. Rodent control in and around the home is essential. Since when working with blood, other biofluids and tissues of sick people and animals, the formation of a virus-containing aerosol is possible, a second level of biological protection must be provided in the laboratory. Patients must be isolated.

(HPS), also known as hantavirus cardiopulmonary syndrome (HPS), while others have not been associated with known disease human. HPS (HCPS) is a "rare respiratory disease associated with inhalation of aerosolized rodent excrement (urine and feces) contaminated with Hantavirus particles."

Human hantavirus infections have been almost entirely associated with human exposure to rodent excrement; in 2005 and 2019 person-to-person transmission of the Andes virus was reported in South America.

Hantavirus pulmonary syndrome

Deer mouse

Hantavirus Pulmonary Syndrome (HPS) is found in North, Central and South America. It is an often fatal lung disease. In the United States, the causative agent is the Nombr Sin virus carried by deer mice. Prodromal symptoms include flu-like symptoms such as fever, cough, muscle pain, headache, and lethargy. It is characterized by the sudden onset of shortness of breath with rapidly developing pulmonary edema, which is often fatal despite mechanical ventilation and powerful diuretics with a mortality rate of 36 percent.

Hantavirus pulmonary syndrome was first detected during an outbreak of 1993 in four corners of the southwestern United States. It was discovered by Dr. Bruce Tempest. It was originally called "Four Corners Disease", but the name was changed to "Sin Nombre Virus" after complaints from Native Americans that the name "Four Corners" stigmatized the region. Since then, it has been identified throughout the United States. Deratization in and around the home remains the main prevention strategy.

virology

classification

Hantaviruses are Bunyaviruses. Bunyaviridae the order is divided into five families: Orthobunyavirus , Nairovirus , phlebovirus , Tospovirus and Hantavirus ... Like all members of this order, Hantaviruses have a genome containing three negative-sense, single-stranded RNA segments, and therefore are classified as negative-sense RNA viruses. Members of others bunyaviruses familiies of the order are usually arthropod-borne viruses, but hantaviruses are thought to be transmitted to humans mainly by inhalation of aerosolized rodent excrement or rodent bites.

genome

Like other members of the bunyavirus family, Hantaviruses are surrounded by viruses with a gene that consists of three single-stranded, negative sensory RNA segments, designated S (small), M (medium), and L (large). RNA S encodes the nucleocapsid (N) of the protein. M RNA encodes a polyprotein that is cotranslationally cleaved to form an envelope of the glycoproteins Gn (formerly G1) and Cc (formerly G2).

L RNA encodes a protein L, which functions as viral transcriptase / replicase. In virions, genomic RNAs from hantaviruses are thought to complex with protein N to form helical nucleocapsids, the RNA component of which circularizes due to sequence complementarity between the 5 "- and 3" - terminal sequences of genomic segments.

As with other bunyaviruses, each of the three segments has a consensus 3 "-terminal nucleotide sequence (AUCAUCAUC), which is complementary to the 5" terminal sequence and distinct from those of the other four genera in the family. These sequences appear to form panhandle structures, which seem to play an important role in the replication and encapsidation of the facilitated viral nucleocapsid (N) protein binding. The large segment is 6530-6550 nucleotides (nt) in length, the medium is 3613-3707 nucleotides in length and the small segment is 1696-2083 nucleotides in length.

No non-structural proteins are known, unlike other genera of this family. The 5 "and 3" of each segment are short non-coding sequences: the non-coding segment in all sequences at the 5 "end is 37-51 nt. 3" non-coding regions differ: L segment 38-43 nt; M segment 168-229 nt; and S segment 370-730 nt. The 3 "end of the S segment persists between births, suggesting a functional role.

Virions

Hantavirus virions are about 120-160 nanometers (nm) in diameter. The lipid bilayer of the viral envelope is about five nm and is embedded with viral surface proteins to which sugar residues are attached. These glycoproteins, known as Gn and Gc, are encoded by the M segment of the viral genome. They tend to bind (heterodimerize) with each other and have both an inner tail and an outer region that extends approximately six nm beyond the envelope surface.

Inside the envelope are nucleocapsids. It consists of multiple copies of the N nucleocapsid protein, which interact with three segments of the viral genome to form helical structures. The virally encoded RNA polymerase is also found in the interior. By weight, the virion is more than 50% protein, 20-30% lipids and 2-7% carbohydrates. The density of virions is 1.18 grams per cubic centimeter. These functions are common to all members of the bunyavirus.

Life cycle

Entry into host cells is believed to occur by attachment to virions by cellular receptors and subsequent endocytosis. Nucleocapsids are introduced into the cytoplasm by pH-dependent synthesis of the virion with the endosomal membrane. After release from the nucleocapsid into the cytoplasm, the complexes target the ER-Golgi. Intermediate compartments (ergic) through microtubular associated movement leads to the formation of viral factories in the ERGIC.

These plants then facilitate the transcription and subsequent translation of viral proteins. Transcription of viral genes must be initiated by the association of the L protein with three nucleocapsid species. In addition to its transcriptase and replicase functions, it is also considered a viral L protein to have endonuclease activity that cleaves cellular messenger RNA (mRNA) to produce blocked primers used to initiate viral mRNA transcription. As a result of this cap snatching, the hantavirus mRNA is capped and contains nontemplated 5 "terminal extensions.

G1 (called Op) and G2 (Gc) glycoproteins form hetero-oligomers and are then transported from the endoplasmic reticulum to the Golgi complex, where glycosylation is complete. The L protein produces the nascent genome from replication using a positive sense RNA intermediate. Hantavirus virions are thought to be harvested by combining nucleocapsids with glycoproteins embedded in Golgi membranes, and then budding into Golgi cisterns. The nascent virions are then transported in secretory vesicles to the plasma membrane and released by exocytosis.

pathogenesis

The pathogenesis of Hantavirus infections is unclear; there is a lack of animal models to describe it (rats and mice do not seem to acquire severe disease). While the main site of viral replication in the body is not known, in HFRS the main effect is in the blood vessels, while in HPS most symptoms are associated with the lungs. In HFRS, there is increased vascular permeability and a decrease blood pressure due to endothelial dysfunction and the most dramatic damage is seen in the kidney, whereas in the HPS, lungs, spleen and gall bladder is the most affected. Early symptoms of HPS tend to present similar to those of influenza ( muscle pain, fever and fatigue) and usually appear about 2 to 3 weeks after infection. Later stages of the illness (about 4 to 10 days after the onset of symptoms) include shortness of breath, shortness of breath, and coughing.

transmission

The species that cause hantavirus hemorrhagic fever have not been shown to be transmitted from person to person. Aerosol rodent transmission of feces is the only known route of transmission to humans. Similar double-stranded RNA viruses, such as Marburg and Ebola haemorrhagic fevers, can be transmitted by contact with infected blood and other body fluids and are known to spread to health workers in African hospitals, although they do not transmit easily to modern conditions hospital with universal precautions. Transmission via fomites has not been demonstrated in hantaviruse disease or in hemorrhagic or pulmonary forms.

evolution

Findings of a significant correspondence between the phylogenies of the hantaviruses and the phylogeny of their rodent reservoirs led to the theory that rodents, although infected virus This is not damaged due to long-standing hantavirus rodent host coevolution, although results in 2008 led to a new hypothesis regarding hantavirus evolution:

Various Hantaviruses have been found to infect several species of rodents, and cases of interspecies transmission (host switching) have been recorded. In addition, substitution rates based on nucleotide sequence data indicate that the Hantavirus clade and rodent subfamily may not have diverged at the same time. In addition, as 2007 hantaviruses have been detected in a large number of species of shrews and moths.

Taking into account the controversy in the theory of coevolution, it was proposed in 2009 that the specimens seen in hantaviruses in relation to their reservoirs could be attributed to preferential host switching under control of geographic proximity and adaptation to specific host types. Another suggestion from 2010 is that geographic clustering of Hantavirus sequences can be triggered by a distance-by-distance isolation mechanism. When comparing hantaviruses found in hosts of the orders Rodentia and shrews, it was proposed in 2011 that hantavirus evolutionary history is a combination of both host switching and codivergence and that hereditary shrews or moles rather than rodents may have been the early original hosts of ancient hantaviruses.

Africa

In 2010, the novel Sangassou hantavirus virus was isolated in Africa, which causes hemorrhagic fever with renal syndrome.

Asia

In China, Hong Kong, Korean Peninsula and Russia, hemorrhagic fever with renal syndrome is caused by Hantaana, Puumal and Seoul viruses.

Australia

In 2005, there were no human infections reported in Australia, although rodents were found to carry antibodies.

Europe

In Europe, three Hantaviruses - Puumala, Dobrava and Saaremaa viruses - are known to cause hemorrhagic fever with renal syndrome. Puumala usually causes a usually mild disease - nephropathia Epidemica - which usually presents with fever, headache, gastrointestinal symptoms, impaired renal function and blurred vision. Dobrava infections while similar often also have hemorrhagic complications. There are several reports of confirmed infections in Saaremaa, but they appear to be similar to those caused by Puumal and less pathogenic than Dobrava.

The Puumal virus is carried by its rodent host, the bank vole ( Clethrionomys glareolus) and is present throughout most of Europe except for the Mediterranean region. Dobrava and Saaremaa viruses are respectively carried out using the yellow necks of mice ( Aroyetiz flavicollis) and field mouse ( Aroyetiz agrarius), reported mainly in eastern and central Europe.

In 2017 alone, the Robert Koch Institute (CRI) in Germany received 1,713 notifications for Hantavirus infections.

The term "hantavirus" represents several groups of RNA viruses (which are members of the virus family Bunyaviridae), which are carried by rodents and can cause severe respiratory infectionscalled hantavirus pulmonary syndrome (HPS) and hemorrhagic fever with renal syndrome (HFRS).

Hantavirus pulmonary syndrome mainly occurs in the Americas (Canada, USA, Argentina, Brazil, Chile, Panama, etc.), while hemorrhagic fever with renal syndrome occurs mainly in Russia, China and Korea, but can be found in Scandinavia and Western Europe, and sometimes in other areas. Like HLS, HFRS develops due to hantaviruses, which are transmitted:

• Urine, droppings or saliva (bite) from rodents;
• By direct contact with animals;
• Dust contaminated with urine or rodent feces;
• If the virus gets into tears in the skin or mucous membranes of the mouth, nose, or eyes.

The overwhelming majority of HPS and HFRS infections are not transmitted from person to person.

The purpose of this article is to discuss HLS; however, much of what is presented with respect to HPS also applies to HFRS - the main difference is that the prevailing symptoms in the later stages of the disease differ somewhat between the two diseases (pulmonary fluid and shortness of breath in HPS and low blood pressure, fever, and renal failure in HFRS).

What is Hantavirus Pulmonary Syndrome?

Hantavirus Pulmonary Syndrome is a disease caused by a hantavirus that causes fluid to fill the human lungs (pulmonary edema) and causes death in about 38% of all infected patients.

What is the history of hantavirus pulmonary syndrome?

The first recognized outbreak of CLS was noted in 1993 in the Four Corners region of the United States, where the states of Arizona, New Mexico, Colorado and Utah meet. Two healthy young men, a Navajo Indian and his fiancée, suddenly suffocated and died. This unusual situation prompted a study of other deaths in four states, which identified five other young people who had recently died with similar breathing problems. Over the next few weeks, other people were found treated in the same area with similar pulmonary syndromes. Tissues from the affected patients were sent to the CDC, where researchers looked for the cause and found a link between the patients: an infection with a previously unknown type of hantavirus.

Further research

Since other known hantaviruses (in Asia and Europe) are known to be transmitted to humans by rodents, researchers began capturing rodents between June and August 1993 to determine if the virus is associated with animals. In November 1993, rodents ( Deer hamster or Peromyscus maniculatus), captured by CDC researchers at a home where a person who developed pulmonary syndrome showed a previously unknown virus. In addition, army researchers soon isolated the same virus from an infected patient who had also had contact with mice. This new hantavirus was first named Muerto Canyon Virus, then Sin Nombre Virus (BCH) and ultimately simply Hantavirus. The disease caused by this virus has been called hantavirus pulmonary syndrome (HPS).

Further research suggested that other people had died from this infection in the past when the virus was found in the autopsy tissue. When Indian Navajo medical traditions were studied, the Navajo medical culture seemed to be familiar with the disease and associated it with mice. The 1993 outbreak likely occurred because environmental factors led to favorable survival and distribution of the mice. In 1993, the mouse population was about ten times that of 1992 in the Four Corners area.

In 2012, Yosemite National Park, California, experienced a large outbreak of HPS. The outbreak was associated with an infection of a deer hamster that infiltrated the camps (tents) used by tourists. At least three deaths have occurred and seven other infected people have recovered.

What Causes Hantavirus Pulmonary Syndrome?

As stated above, HPS is caused by infection of the patient with hantavirus. Currently, about 14 subtypes of hantaviruses have been identified. Many subtypes have been named (eg, Sin Nombre virus, Black Stream Hantavirus, and New York Hantavirus); some researchers simply put them under the term "New World hantaviruses." The Sin Nombre subtype summoned most current diseases of HLS. The virus apparently damages the cells that form the capillaries blood vesselscausing fluid to leak. This leakage of fluid, if deep in the lungs, causes pulmonary syndrome that can be fatal.

Hantaviruses live their life cycle in rodents, but do not seem to harm them. Viruses multiply and enter rodent urine, feces and saliva. A recent study in California found that about 15% of all deer hamsters tested tested positive for hantavirus. Although the deer hamster has been the source of most HPS infections, many other rodents can carry a different virus of the hantavirus subtype (eg, white-footed hamster, cotton hamsters, and swamp rice hamster).

What are the risk factors for Hantavirus Pulmonary Syndrome?

The main risk factor for Hantavirus Pulmonary Syndrome is contact with rodents, their saliva, urine or feces, or dust, dirt, or surfaces contaminated with such objects, either by direct contact or aerosol. Sheds, sheds, houses or buildings easily accessible by rodents are potential sites for hantavirus infection. Rural areas that have forests and fields that can support a large rodent population are areas that increase the risk of HPS infection. Camping and hiking in areas known to have high rodent populations and where rodents may seek refuge increases the risk. Those who work in areas that may provide shelter for rodents (eg, crawling, clearing buildings, construction sites) may also be at increased risk of developing CLS. The risk is also higher in people who work in areas that have previously had HPS infections.

Is hantavirus contagious?

Hantavirus is not contagious and cannot be transmitted from person to person. The virus is transmitted from rodents to humans. Outbreaks usually occur in groups of people exposed to the same infected rodents; but those who have hantavirus infections do not transmit them to other uninfected people. Although there is a situation in North America, there are reports that in 1996 a moderate infection with hantaviruses was transmitted as a result of an outbreak in Argentina. However, no human-to-human transmission of the virus has been reported to date. Small outbreaks reported every year; for example, Texas had the first person to be diagnosed with hantavirus in 2015.

How long is the infectious period of Hantavirus?

There is no evidence in North America that hantavirus is contagious. In South America, an estimated 16-35 days was an infectious period for several patients who, according to investigators, showed person-to-person transmission.

What is the incubation period for hantavirus?

In North America, the incubation period (the time from initial exposure to the virus to the development of the first symptoms) is estimated to range from one to five weeks after the initial exposure to infected urine, droppings, or rodent saliva, according to the CDC. In South American outbreaks, researchers believe that incubation period ranges from 12 to 27 days.

What are the signs and symptoms of hantavirus pulmonary syndrome?

The symptoms and signs of CLS are usually grouped into early and late stages. The early signs and symptoms of CLS begin approximately one to five weeks after human exposure to hantavirus associated with rodent urine, feces, or saliva. Early symptoms last four to ten days and include the following:

• Fatigue;
• Fever;
• Muscle pain (especially the muscles in the legs, back and hips).

Almost every infected person has these symptoms. Other symptoms that can occur in about half of infected patients include abdominal pain, nausea, vomiting and diarrhea, headaches, chills, and dizziness.

Late symptoms of CLS occur approximately 4-10 days after the onset of early symptoms and include cough, chest pain, and shortness of breath, which can become severe.

How is Hantavirus Pulmonary Syndrome Diagnosed?

There are currently no tests available to diagnose HPS or even hantavirus infection for early stage infections or diseases are mainly due to the fact that the early symptoms are so nonspecific and the disease of HPS is so rare. There was no pressing need for a test. However, if a more severe HPS disease develops, the disease is presumably diagnosed by an association of doctors in the area where the rodents breed, or in places where HPS is known to exist. Sequential radiographs chest may show deteriorating changes and an increase in the amount of fluid. The final diagnosis is usually carried out by special laboratories using special immunological tests that can distinguish hantavirus from Ebola, from Marburg and other viruses.

Figure 2: Chest X-ray of a Patient with Hantavirus Pulmonary Syndrome (HPS);

How did viruses come about? Who invented them why are they not taking the lives of thousands of people around the world every year? There are drugs against the worst viruses in the world and how to protect yourself from terrible diseases? We present to your attention the rating of the most dangerous viruses.

1. Human immunodeficiency virus

Human immunodeficiency virus (HIV) is the most dangerous human virus, the causative agent of HIV / AIDS, which is transmitted through direct contact of mucous membranes or blood with bodily fluid of the patient. In the course of HIV infection, all new strains (varieties) of the virus are formed in the same person, which are mutants, completely different in reproduction speed, capable of initiating and killing certain types of cells. Without medical intervention, the average life expectancy of a person infected with the immunodeficiency virus is 9-11 years. According to the data for 2011, 60 million people in the world fell ill with HIV infection, of which 25 million died, and 35 million continue to live with the virus.

2. Marburg virus

The most dangerous virus that a person can contract is the Marburg virus. It is named after the small, idyllic town on the Lahn River where an outbreak of the disease was first reported and described. It is very similar to the Ebola virus: sufferers suffer from febrile convulsions and bleeding from the mucous membranes, skin and organs. 80 percent of those infected die.

3. Ebola virus

The Ebola virus can manifest itself in five different types, which have been named after countries and regions in Africa: Zaire, Sudan, Tai Forest Ebolavirus, Bundibugio, Reston. The Zaire type Ebola virus is the most dangerous, as the mortality rate of people infected with it reaches 90 percent. It was he who infected people in Guinea, Sierra Leone and Liberia during the 2013 Ebola epidemic. Researchers believe that bats brought the virus to cities from Zaire.

4. Hunt virus

Hunt virus covers wide range viruses. It bears the name of the river where American soldiers were first infected with the virus during the Korean War in 1950. Symptoms of the virus include lung disease, fever, and kidney failure.

5. Hantaviruses

Hantaviruses are a genus of viruses transmitted to humans through contact with rodents or their metabolic products. Hantaviruses cause various diseasesrelated to such groups of diseases as “hemorrhagic fever with renal syndrome” (mortality rate on average 12%) and “hantavirus cardiopulmonary syndrome” (mortality rate up to 36%). The first major outbreak of the disease caused by hantaviruses, known as "Korean hemorrhagic fever", occurred during the Korean War (1950-1953). Then more than 3,000 American and Korean soldiers felt the impact of a then unknown virus that caused internal bleeding and impaired kidney function. Interestingly, this particular virus is considered the likely cause of the outbreak in the 16th century, which exterminated the Aztec people.

6. Lassa virus

A nurse in Nigeria was the first person to contract the Lassa virus. The spread of the virus carried by rodents was endemic; very active, but in a specific region, in this case in West Africa. Even now, the virus is raging again in Nigeria. Researchers suspect that 15 percent of the rodents living there are carriers of the virus.

7. Rabies virus

The rabies virus is a dangerous virus that causes rabies in humans and warm-blooded animals, in which a specific lesion of the central nervous system... This disease is transmitted through saliva when bitten by an infected animal. Accompanied by an increase in temperature to 37.2-37.3, bad sleep, patients become aggressive, violent, hallucinations, delirium, a feeling of fear appear, paralysis of the eye muscles soon occurs, lower limbs, paralytic breathing disorders and death. The first signs of the disease appear late, when destructive processes have already occurred in the brain (edema, hemorrhage, degradation of nerve cells), which makes treatment almost impossible. To date, only three cases of human recovery have been recorded without the use of vaccination, all the rest ended in death.

8. Smallpox virus

The smallpox virus is a complex virus, the causative agent of the highly contagious disease of the same name that affects only humans. This is one of the oldest diseases, the symptoms of which are chills, pain in the sacrum and lower back, a rapid increase in body temperature, dizziness, headache, vomiting. On the second day, a rash appears, which eventually turns into purulent blisters. In the 20th century, this virus claimed the lives of 300-500 million people. The smallpox campaign spent about US $ 298 million between 1967 and 1979 (the equivalent of US $ 1.2 billion in 2010). Fortunately, the last known case of infection was reported on October 26, 1977 in the Somali city of Marka.

9. Rotavirus

The ninth place in the list of the most dangerous human viruses is occupied by Rotavirus - a group of viruses that are the most common cause acute diarrhea in infants and young children. It is transmitted by the fecal-oral route. The disease is usually easy to treat, but more than 450,000 children under the age of five die each year worldwide, most of whom live in underdeveloped countries.

10. Influenza virus

Influenza virus is a virus that causes acute infection respiratory tract... Currently, there are more than 2 thousand variants of it, classified into three serotypes A, B, C. A group of the virus from serotype A divided into strains (H1N1, H2N2, H3N2, etc.) is the most dangerous for humans and can lead to epidemics and pandemics. Every year in the world, from 250 to 500 thousand people die from seasonal flu epidemics (most of them are children under 2 years of age and elderly people over 65).

Hantavirus infection is a dangerous, sometimes fatal, infectious disease caused by the hantavirus.

Hantavirus is a distant relative of the virus that causes Ebola. It can cause respiratory failure in infected people. Hantavirus is known to have caused disease in China for many years.

Hantavirus infection usually requires hospitalization and intensive care. Among the diagnosed diseases, the mortality rate reaches 50%.

Other names for hantavirus infection are hantavirus, hantavirus pulmonary syndrome, HLS.

Symptoms

Symptoms and signs of hantavirus infection include:

• Fatigue;
• Temperature;
• Muscle pain, especially in the hips and back;
• Headache;
• Dizziness;
• Nausea, vomiting, abdominal pain;
• Cough;
• Severe shortness of breath.

As with many other infections early signs and HPS symptoms are similar to those of influenza. Almost every patient first has a fever, increased fatigue and muscle pain, especially in the hips, back and sometimes shoulders.

About half of people who get sick have headaches, dizziness, chills and abdominal problems such as nausea, vomiting, diarrhea, and abdominal pain.

Symptoms may improve, but coughs and shortness of breath appear after 1–2 days as the lungs fill with fluid. Breathing difficulties may be mild at first, but then rapidly deteriorate. Internal bleeding occurs, followed by respiratory failure.

See your doctor right away if you have had contact with rodents and suddenly have flu-like symptoms or shortness of breath. Inform your doctor about your exposure to rodents so that they can assume the possibility of a hantavirus infection. When treatment is started on time, the chances of recovery increase.

Causes

The causative agent of hantavirus infection is hantavirus.

The carriers of the virus in nature are rodents: bank voles, field mice, gray and black rats, white-footed hamsters and cotton rats. Other animals (cats, dogs, livestock) and insects do not carry the virus. A person cannot transmit the virus to another person.

The virus does not cause disease in rodents. It is excreted in their saliva, urine and feces. Presumably, people become infected by inhaling air contaminated with rodent secretions. This can happen when cleaning barns, barns, attics and other areas where infected rodents have lived, when infected dust rises into the air.

Diagnostics

In addition to blood tests, a chest x-ray may be done to look for changes in the lungs.

Treatment

Effective methods there is currently no treatment for HLS. In case of respiratory disorders, oxygen therapy or artificial ventilation of the lungs is prescribed. Treatment is ineffective in very severe cases.

Prevention

There is no vaccine for hantavirus.

The best way ChPS prevention - avoid contact with feces, urine and rodent nests. At home, you need to get rid of rodents using mousetraps and covering up holes that can lead to burrows.

At picnics or camping out in nature, do not pitch tents in areas with mouse feces. Underlay a tarp to avoid direct contact with potentially contaminated dust. Ventilate and disinfect areas before settling in.

When cleaning a barn or barn that may contain rodents, be guided by following recommendations:

• Wear rubber gloves and, if possible, surgical masks.
• Do not vacuum or sweep faeces, urine, or nesting material as this may raise contaminated dust.
• Ventilate the area 30 minutes before starting cleaning. Leave it while airing.
• Spray the area with disinfectant. Then leave for another 30 minutes.
• Thoroughly dampen rodent droppings and nesting material with 10% chlorine solution or similar disinfectant and leave wet for 30 minutes. Put on rubber gloves, put it in a plastic bag, close it tightly and throw it away or burn it. Do the same with the gloves.
• Wash any suspected contaminated surfaces with a disinfectant. Do not turn on the vacuum cleaner until thoroughly cleaning the area, and after that do it only with ventilation.