Wednesday, October 17, 2018

What is a influenza virus? What are the routes of transmission, diagnostic methods, and preventive measures for influenza viruses?

What is a influenza  virus? What are the routes of transmission, diagnostic methods, and preventive measures for influenza viruses?
What is a influenza  virus? What are the routes of transmission, diagnostic methods, and preventive measures for influenza viruses?
Introduction to influenza virus
Influenza virus is a representative species of Orthomyxoviridae, abbreviated as influenza virus, including human influenza virus and animal influenza virus. Human influenza virus is divided into three types: A, B, and C. It is influenza. The pathogen of (flu). Among them, the antigenicity of influenza A virus is prone to mutation, causing a worldwide pandemic many times. For example, in the 1918-1919 pandemic, at least 20 million to 40 million people worldwide died of influenza; influenza B virus is also more pathogenic to humans, but people have not found that influenza B virus has caused worldwide A pandemic; influenza C virus causes only insignificant or mild upper respiratory tract infections in humans and rarely causes epidemics. Influenza A virus was successfully isolated in 1933, influenza B virus was acquired in 1940, and influenza C virus was not successfully separated until 1949.

Influenza classification

According to the target of influenza virus infection, the virus can be divided into human influenza virus, swine influenza virus, equine influenza virus and avian influenza virus. The human influenza virus can be divided into three categories according to the antigenicity of its nuclear protein:
Influenza A virus, also known as influenza A virus
Influenza B virus, also known as influenza B virus
Influenza C virus, also known as influenza C virus
Influenza viruses that infect other animals such as birds and pigs have the same antigenicity as the human influenza A virus, but since the classification of influenza A, B and C viruses is only for human influenza viruses, it is usually not An influenza virus other than a human host such as avian influenza virus is referred to as an influenza A virus.
Based on the antigenicity of nuclear proteins, influenza viruses are also classified into different subtypes based on the antigenicity of hemagglutinin HA and neuraminidase NA.


Morphology

The influenza virus is spherical, and the newly isolated strains are mostly filamentous, with a diameter between 80 and 120 nanometers, and a filamentous influenza virus with a length of up to 4000 nanometers.
The structure of influenza virus can be divided into envelope, matrix protein and core three parts from the outside.

Core
The core of the virus contains the genetic material that stores the virus information and the enzymes necessary to replicate the information. The genetic material of influenza virus is a single-stranded negative-strand RNA, abbreviated as ss-RNA. The ss-RNA is combined with nuclear protein (NP) and entangled into ribonucleoprotein body (RNP), which exists in extremely high density. In addition to ribonucleoproteins, there are RNA polymerases responsible for RNA transcription.
The RNA of influenza A and B viruses consists of 8 segments, the influenza C virus is one segment less than them, and the 1st, 2nd, and 3rd segments encode RNA polyaggregates, the fourth segment. Responsible for encoding hemagglutinin; the fifth segment is responsible for encoding nuclear proteins, the sixth segment encodes neuraminidase; the seventh segment encodes matrix proteins, and the eighth segment encodes a To the non-structural proteins that spliced ​​RNA function, the other functions of this protein are still unknown.
The lack of influenza C virus is the sixth segment, and the hemagglutinin encoded by the fourth segment can simultaneously function as a neuraminidase.

Matrix protein
The matrix protein constitutes the outer shell skeleton of the virus, and in fact, in addition to the matrix protein (M1), the membrane protein (M2). The M2 protein has an ion (mainly Na+) channel and regulates the pH in the membrane, but in a small amount. The tight binding of the matrix protein to the outermost envelope of the virus serves to protect the viral core and maintain the spatial structure of the virus.
After the influenza virus completes its reproduction in the host cell, the matrix protein is distributed on the inner wall of the host cell membrane, and the shaped viral nucleocapsid recognizes the site containing the matrix protein on the host cell membrane, and combines to form a viral structure, and The budding form highlights the release of the mature virus.

Envelope
The envelope is a layer of phospholipid bilayer membrane wrapped outside the matrix protein. This membrane is derived from the host cell membrane. The mature influenza virus buds from the host cell, and the host cell membrane is wrapped in the body and then detached from the cell to infect. Next target.
In addition to phospholipid molecules, there are two very important glycoproteins in the envelope: hemagglutinin and neuraminidase. These two types of proteins protrude from the virus in vitro and are about 10 to 40 nanometers in length and are called spikes. Generally, an influenza virus surface is distributed with 500 hemagglutinin spikes and 100 neuraminidase spikes. The antigenicity of hemagglutinin and neuraminidase changes in influenza A virus, which is the basis for distinguishing virus strain subtypes.

Hemagglutinin (HA)
It is columnar and can bind to receptors on the surface of red blood cells of animals such as humans, birds, and pig guinea pigs to cause blood clotting, so it is called hemagglutinin. After hemagglutinin proteolysis, it is divided into two parts: light chain and heavy chain. The latter can bind to the sialic acid receptor on the host cell membrane, and the former can assist the fusion of the viral envelope and the host cell membrane. Hemagglutinin plays an important role in the introduction of the virus into host cells. Hemagglutinin is immunogenic and anti-hemagglutinin antibodies neutralize influenza viruses.

Neuraminidase (NA)
It is a mushroom-like tetrameric glycoprotein with the activity of hydrolyzing sialic acid. When the mature influenza virus is budded out of the host cell, the hemagglutinin on the surface of the virus will keep in contact with the host cell membrane via the sialic acid receptor. It is necessary to hydrolyze sialic acid by neuraminidase, and cut off the last connection between the virus and the host cell, so that the virus can be smoothly released from the host cell, and then the next host cell is infected. Therefore, neuraminidase has also become a target for influenza treatment drugs, and oseltamivir designed for this enzyme is one of the most famous anti-influenza drugs.

Naming method
According to the amendments to the nomenclature of influenza virus strains adopted by the World Health Organization in 1980, the naming of influenza strains contains six elements: type/host/separation area/strain number/year of isolation (HnNn), for human influenza virus The host information is omitted, and the subtype information is omitted for the influenza B and C viruses. For example, A/swine/Lowa/15/30 (H1N1) indicates that the nuclear protein is type A, and the pig-hosted H1N1 subtype influenza virus strain isolated in lowa in 1930 has a strain number of 15, which is It is also the first strain of influenza virus isolated from humans.

Virus variation
Influenza virus variants have variations in antigenic variation, temperature-sensitive variation, host range, and sensitivity to non-specific inhibitors, but the most important are antigenic variations. The antigenic variation is different from other viruses, and the surface antigens HA and NA are susceptible to mutation. There are two forms of variation, namely antigenic transformation and antigenic drift.
The magnitude of the variation of the surface antigen of influenza virus directly affects the scale of influenza. If the variation is small, it is a quantitative change, called antigen drift, and a virus-producing strain can cause small and medium-sized epidemics. If the antigen variability is large, it is a qualitative change, called an antigenic transformation, forming a new subtype. At this time, the population generally lacks immunity to it, often causing a large epidemic, and even a worldwide epidemic. For example, HA and NA of influenza A virus are prone to antigenic transformation, which constitutes HA. Most or all of the amino acids of NA can be changed, and new subtypes with completely different antigenicity appear. The variation is changed from quantitative to qualitative. When new influenza virus subtypes emerge, the population is generally immune to it and is therefore prone to pandemics.

Antigenic transformation
The antigenic shift has a large variation and belongs to the qualitative change. That is, one or two of the surface antigen structures of the virus strain are mutated, which is different from the antigen of the previous epidemic strain, forming a new subtype (such as H1N1→H2N2, H2N2→H3N2). ), because the population lacks immunity to the mutant strain, causing a pandemic. If two different viruses simultaneously infect the same cell, genetic recombination can occur to form a new subtype. The H3N1 subtype was isolated from the simultaneous infection of the influenza A virus H1N1 in the Soviet Union in 1978 and the H3N2 influenza A virus in Hong Kong, indicating that such variation can occur in a natural epidemic. In the past, it has been thought that the alternation between old and new subtypes of viruses is rapid. Once the new subtypes appear, the old subtypes will soon disappear. However, in 1997, although Hagar 1 (H1N1) reappeared, it has not yet replaced Al 3 (H3N2), but both are popular. Until 1998, the antigen of the representative strain of type A (H3N2) was mutated, and the Wuhan strain was replaced by the Sydney strain. People were not immune to the new strain, which caused a new epidemic.

Antigenic drift
The antigenic drift variation is small or continuous, and is a quantitative change, that is, intra-subtype variation. It is generally believed that this mutation is caused by viral gene point mutations and population immunity selection, and the resulting epidemics are small-scale.
Among the three influenza viruses that infect humans, influenza A virus has a strong variability, followed by type B, while the antigenicity of influenza C virus is very stable.
The mutation of influenza B virus will produce a new mainstream strain, but there is cross-immunization between the new strain and the old strain, that is, the immune response against the old strain is still effective for the new strain.
Influenza A is one of the most mutated types. Every fifteen years, an antigenic mutation occurs, producing a new strain. This change is called antigenic change, also known as antigenic change; in influenza A Small variations in the antigen also occur in the subtype, and its manifestation is mainly a point mutation of the antigenic amino acid sequence, which is called antigenic drift, also known as the amount of antigen. The antigenic transformation may be a simultaneous transformation of the hemagglutinin antigen and the neuraminidase antigen, called a large family variation; it may also be only a hemagglutinin antigen mutation, while the neuraminidase antigen does not change or only a small mutation occurs, called Subtype variation.
For the variability of influenza A virus, there is no unified understanding in the academic world. Some scholars believe that it is because the influenza A virus circulating in the population faces greater immune pressure, which causes the virus nucleic acid to continually mutate. Other scholars believe that the mutation of the virus caused by genetic recombination of human influenza A virus and avian influenza virus simultaneously infected pigs. The views of the latter scholars were supported by some facts. Laboratory work showed that three of the eight segments of the popular Asian influenza virus (H2N2) gene in 1957 were from the duck flu virus, while the remaining five segments were from H1N1 human influenza virus.
The high variability of influenza A virus increases the difficulty of people responding to influenza. People cannot accurately predict the upcoming viral subtypes, and they cannot carry out targeted preventive vaccination. On the other hand, every tenth The antigenic transformation that occurs in the year will result in a new strain of influenza that has no vaccine at all.

Breeding method
Influenza virus can proliferate in the amniotic cavity and allantoic cavity of chicken embryos. The proliferating virus is freed from amniotic fluid or allantoic fluid and can be detected by a red blood cell agglutination test. Although the influenza virus can proliferate in tissue culture cells (human amniotic membrane, monkey kidney, dog kidney, chicken embryo, etc.), it does not cause significant CPE, and the red blood cell adsorption test can be used to determine the presence or absence of virus proliferation. Susceptible animals are ferrets, and continuous passage of the virus in mice can increase virulence and cause extensive substantial lesions or death in the lungs of mice.

Main characteristics
The flu virus is weakly resistant and not heat-resistant, and the virus can be inactivated at 133℉ for 30 minutes. Infectivity is quickly lost at room temperature, but it can survive for several weeks at 32℉ ~ 39℉, and can survive for a long time after -158℉ or after lyophilization. The virus is also sensitive to dry, sunlight, ultraviolet light, and chemicals such as ether, formaldehyde, and lactic acid.

Way for spreading
The source of infection is mainly patients, followed by latent infections, and infected animals may also be a source of infection. The main route of transmission is droplets with influenza virus that enter the body through the respiratory tract. A small number can also be infected by indirect contact with handkerchiefs, towels, etc.
After the virus is introduced into the population, it is highly contagious and can spread rapidly. The speed and breadth of transmission are related to population density. Viruses entering the human body, if not cleared by cough reflexes, or not neutralized by specific IgA antibodies in the body and non-specific inhibitors in mucosal secretions, can infect a small number of airway epithelial cells, causing cells to produce vacuoles and denaturation And the progeny virion rapidly spreads to adjacent cells, and the virus proliferation cycle is repeated. The NA of the virus reduces the viscosity of the mucous layer of the respiratory tract, not only exposes the cell surface receptors, but also promotes the adsorption of the virus, and also promotes the distribution of the virus-containing liquid to the lower respiratory tract, which damages many respiratory cells in a short period of time. Influenza viruses generally cause only surface infections and do not cause viremia.
The target of influenza virus invasion is respiratory mucosal epithelial cells, and occasionally cases of invasion of the intestinal mucosa can cause gastrointestinal influenza.
After invading the body, the virus is adsorbed on the surface of the host cell by hemagglutinin, and is swallowed into the cytoplasm; after entering the cytoplasm, the viral envelope fuses with the cell membrane to release the contained ss-RNA; the eight segments of the ss-RNA are in the cytosol Internal coding RNA polymerase, nuclear protein, matrix protein, membrane protein, hemagglutinin, neuraminidase, non-structural protein and other components; matrix protein, membrane protein, hemagglutinin, neuraminidase and other encoded proteins in the endoplasmic reticulum Or M-protein and capsule are assembled on the Golgi; in the nucleus, the genetic material of the virus continuously replicates and forms a viral core with nuclear proteins, RNA polymerase, etc.; the final virus core binds to the M protein and envelope on the membrane, and is released by budding. Outside the cell, the cycle of replication is approximately 8 hours.
Influenza virus infection will cause degeneration, necrosis and even shedding of host cells, resulting in mucosal congestion, edema and increased secretions, resulting in nasal congestion, runny nose, sore throat, dry cough and other symptoms of upper respiratory tract infection. When the virus spreads to the lower respiratory tract, it may be Causes bronchiolitis and interstitial pneumonia.
The population is generally susceptible, and the length of the incubation period depends on the amount of virus invaded and the immune status of the body, usually 1 to 4 days. After onset, the patient has symptoms such as chills, headache, fever, soreness, fatigue, nasal congestion, runny nose, sore throat and cough. Within 1 to 2 days of the onset of symptoms, the amount of virus excreted with the secretions is large, and then rapidly decreases. Uncomplicated patients begin to recover on the 3rd to 4th day after onset; if there is a complication, the recovery period is prolonged. The flu is characterized by high morbidity and low mortality, and death is usually caused by concurrent bacterial infections. Common bacteria include Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, and the like. Complications are more common in infants, the elderly and patients with chronic diseases (cardiovascular disease, chronic bronchitis and diabetes).

Diagnosis method
Viral infection also induces interferon expression and cellular immunomodulation, causing some autoimmune reactions, including high fever, headache, gastrocnemius and systemic muscle pain. Toxin-like products of virus metabolism and cell necrosis release products can also cause and aggravate the above reactions. .
Since influenza virus infection can reduce the ability of respiratory mucosal epithelial cells to clear and adhere to foreign bodies, it greatly reduces the body's ability to resist respiratory infections. Therefore, influenza often causes secondary infections. Secondary pneumonia caused by influenza is flu-killed. One of the main causes of death.
It is not difficult to diagnose influenza in combination with clinical symptoms during the epidemic period, but laboratory tests must be performed for diagnosis or epidemiological surveillance, including virus isolation, serological diagnosis and rapid diagnosis.

Virus isolation and identification
Usually take the pharyngeal lotion or throat swab of the patient within 3 days after the onset of the disease. After antibiotic treatment, inoculate it in the amniotic cavity and allantoic cavity of chicken embryos of 9-11 days old. After incubating for 3 to 4 days at 91 ℉ ~ 95 ℉, amniotic fluid is collected. Hemagglutination test was performed with allantoic fluid. If the hemagglutination test is positive, hemoagglutination inhibition (HI) test is performed with known immune serum to identify the type. If the hemagglutination test is negative, the chicken embryo is then blindly passaged for 3 times, and blood coagulation is still not observed to determine that the virus is negative. The virus can also be isolated by tissue culture cells (such as human embryonic kidney or monkey kidney), and the presence or absence of virus proliferation can be determined by the erythrocyte adsorption method or the fluorescent antibody method.

Serological diagnosis
Take the sera from the acute phase of the patient (within 5 days of onset) and the recovery phase (2 to 4 weeks of disease), and use the HI test to detect antibodies. A diagnosis can be made if the recovery period is more than four times higher than the serum antibody titer in the acute phase. Normal human serum often contains non-specific inhibitors, so serum can be treated with trypsin or the like before the HI test, so as not to affect the HI test results. The virus used in the HI test should be a virus strain closely related to the current epidemic, and the reaction results can be exact. Complement fixation (CF) can only detect antibodies against NP and MP. These antibodies appear early and disappear quickly. Therefore, the CF test can only be used as an indicator of whether it is a recent infection.

Quick diagnosis
Rapid diagnosis of patients, mainly by indirect or direct immunofluorescence, ELISA detection of viral antigens. The patient's turbinate mucosa or respiratory tract epithelial cell smear is often taken, and the antigen is detected by immunofluorescence staining with fluorescein-labeled influenza virus immune serum, or the antigen in the pharyngeal sputum is examined by ELISA. The monoclonal antibody can be used to rapidly detect viral particles or virus-associated antigens of infected influenza A and B viruses in infected cells by immunoenzymatic labeling for only 24 to 72 hours.
Methods such as PCR, nucleic acid hybridization or sequence analysis are also used to detect influenza virus nucleic acids or to perform typing.

Precaution
How to prevent influenza
Influenza is an acute respiratory infection caused by the flu virus, and there is no specific antiviral drug. Early detection and early medication can achieve better results. How to prevent it?

1. Improve your own immunity.
You can improve your body's immunity and fight the virus by exercising your body. Normal work, life, learning should be combined with work and rest, excessive fatigue, resulting in decreased resistance, highly susceptible to viral influenza. Strengthen nutrition, a balanced diet, diet should be light, eat more vegetables and fruits rich in high vitamins, children should not eat cold drinks.

2. Insist on washing your face with cold water to enhance the ability of the nasal mucosa to adapt to the air. Keep abreast of the weather changes and keep warm according to the weather. At the same time, strengthen physical exercise, enhance the ability to adapt to the environment and the body's immunity. In addition, during the cold epidemic, try to go to places with dense population and wash your hands frequently. When the body is slightly uncomfortable, mild dry mouth, take the medicine immediately when the nose is stuffed, drink plenty of water, pay attention to keep warm and rest, so that the condition will improve in time.

3. Air conditioner should be cleaned before using air conditioner to avoid a large number of germs blowing out with the wind; room temperature should be controlled above 74 ℉, keep the indoor and outdoor temperature difference not more than 45 ℉, avoid the burden of body temperature adjustment center; pay attention to air conditioning during sleep or Do not blow the head directly on the fan.

4. In summer, sweating and consumption are large, and sufficient nutrition should be added to improve the body's resistance. Appropriate consumption of fish, meat, eggs, milk and beans to supplement protein, eat more fresh fruits and vegetables to take vitamin C, and eat more hot and humid food, such as bitter gourd, peach, cucumber, mung bean and so on.

5. After taking preventive drugs, the incidence of colds can generally be reduced by about 50%. In addition, people with weak constitutions can also be vaccinated in advance to prevent colds.

6. Pay attention to hygiene
Hygiene should be taken care of to prevent illness from entering the mouth. Wash hands frequently, take a shower, change clothes, diligently and be smashed, and the room is often ventilated. If you have a cold patient, pay attention to keep the distance! In the high season of colds, try to be as small as possible.

7. Learn relevant knowledge
Understand the prevention and prevention of influenza, find a cold to seek medical treatment in time, so as not to delay the disease, but also need to stay in bed, pay attention to keep warm, reduce activities, drink plenty of water.

Method of preventing influenza
The bed sheets should be washed frequently, and the quilt should be exposed to the sun in the sun to kill harmful bacteria. In places with dense crowds, it is best to wear a mask (prefer not to go); keep the air circulation in the room, often open the window. Keep the room clean and hygienic; climate change is very fast, remember to increase or decrease clothing, be careful of colds; enhance physical fitness, exercise, do some aerobic exercise, enhance body immunity; when you come back, remember to wash your hands, try not to touch dirty hands Eyes, nose, mouth; diet is light, don't eat too much spicy and cold food. For antiviral treatment, we have localized oseltamivir phosphate. Compared with imported drugs, its efficacy is safe. And Kewei not only has a capsule dosage form, but also innovatively developed a granule type for children to take. When is the flu vaccine? The flu vaccine is best vaccinated in the fall, because the temperature changes greatly in autumn and winter, and it is the high incidence of flu. After the winter, when the spring blooms, the flu will disappear. A shot can generally be used for half a year. After half a month of vaccination, it can produce viral antibodies, enhance human immunity, avoid getting sick at the peak of the flu, and pay attention to the vaccine. At the peak of the flu, remember to pay more attention. Rest, light diet, enhance physical fitness, exercise.

Prevention
Integrated prevention
On the one hand, prevention and treatment of influenza virus should strengthen the detection of influenza virus mutation, try to make accurate predictions for targeted vaccination; on the other hand, cut off the spread of influenza virus in the population. The influenza virus relies on droplet infection to detect it as soon as possible. Influenza patients, the use of chemical disinfectants in public places fumigation and other means can effectively inhibit the spread of influenza virus; for influenza patients, can be treated with drugs such as interferon, amantadine, oseltamivir, interferon is a kind of inhibition The virally replicating cytokine, amantadine, acts on the influenza virus membrane protein and hemagglutinin protein, preventing the virus from entering the host cell, and oseltamivir inhibits neuraminidase activity and prevents the mature virus from leaving the host cell. There are also indications that Chinese medicines such as Radix Isatidis and Folium Isatidis may have the activity of inhibiting influenza virus, but it has not been confirmed by experimental facts. In addition to treatment for influenza viruses, more treatments are directed against symptoms caused by influenza viruses, including non-steroidal anti-inflammatory drugs, which can alleviate flu symptoms but do not shorten the course of the disease.
Influenza is the abbreviation of influenza. It is an acute respiratory infection caused by influenza virus. It spreads through droplets and is essentially different from the common cold. It is very harmful to people's health.
Although, people all year round may be attacked by the flu virus. But winter is a high season. In winter, the weather is cold, the body's resistance is weakened, and it is easy to get cold. In addition, people spend most of their time indoors, windows are often closed. The air is not circulating, and the virus is more likely to spread. In addition, the winter climate is dry, the body's respiratory system is less resistant, and it is easy to cause or aggravate the respiratory diseases.
In fact, as long as we exercise the right amount of exercise, pay attention to a reasonable diet, and enhance the body's resistance, the flu is completely preventable. The following is the way to enhance immunity and resist the flu virus diet.

Diet therapy
Drink plenty of water to keep the mucous membranes in the mouth and nasal cavity moist, and effectively function to remove bacteria and viruses.
Eat more protein-rich foods
The main substance of the human immune system is immunoglobulin. When the human body lacks protein, the number of lymphocytes in the immune cells is greatly reduced, and the synthesis of immune substances is insufficient, resulting in a serious decline in immune function. Protein is mainly obtained from animal foods such as beef, peeled chicken breast, egg white, milk, shrimp, etc.
Eat more iron-containing foods
Iron-rich food studies have found that people with iron deficiency have lower immunity. When the iron content in the human body is insufficient, the content of T cells that play a regulatory role in the immune system will decrease, and the immune system will not function effectively. In addition, iron is an important component of hemoglobin. Increased iron intake can promote the synthesis of hemoglobin, promote peripheral circulation, and avoid cold hands and feet. Because the foot is sensitive to temperature, if the foot is cold, it will reflexively cause contraction of the nasal mucosa, making people vulnerable to influenza virus. Iron-rich foods mainly include animal liver, meat, pig blood, duck blood, eggs, and dark vegetables.
Eat more zinc-containing foods
Zinc-rich food zinc activates more than 200 hormones and enzymes important to life, helping the immune system to maximize its defense. Zinc deficiency can reduce the level of immunoglobulins in the body, leading to a weakened body's ability to prevent, increasing the chances of various epidemics including the flu. Zinc-rich foods mainly include oysters, crabs, beans, beef, lamb, dried fish, scallops, pork liver, and wheat germ.

Vitamin
Vitamin A can maintain the stability of respiratory mucosal epithelial cells. Vitamin C and Vitamin E are antioxidants that are naturally found in foods. They can remove free radicals that are harmful to our body and enhance our body's resistance. B vitamins participate in energy metabolism in the body, promote protein synthesis, and play an important role in the normal maintenance of physiological functions. These vitamins are abundant in vegetables, fruits, cereals, and beans.

Self-healing method
The human body can produce specific cellular and humoral immunity after infection with influenza virus or after vaccination. Anti-HA and anti-NA are specific antibodies to influenza. Anti-HA is a neutralizing antibody, so the resistance to infection is related to anti-HA, while reducing the disease and preventing the spread of the virus is related to anti-NA. Anti-NP is type-specific and can only be used for the isolation of virus. Serum antibodies and sIgA antibodies in nasal secretions are involved in protection, and local secretory antibodies may be the most important factor in preventing infection. People with certain antibody titers can be infected but mild. The three types of influenza viruses are not associated with the antigen and therefore cannot induce cross protection. When the type of a virus undergoes an antigenic drift, a person with a high antibody titer against the strain may have a mild infection with the new strain. Serum antibodies can last for months to years, while secretory antibodies persist for a short period of time, usually only a few months. The cellular immune response is mainly that specific CD4+ T lymphocytes can help B lymphocytes to produce antibodies, CD8+ T cells can dissolve infected cells, reduce the amount of virus in the lesion, and contribute to the recovery of the disease. It is worth noting that the CD8+ T cell response is cross-over (which can dissolve cells infected by any strain), does not have plant specificity, and may act directly on viral nucleoproteins rather than on virion surface glycoproteins.
Influenza A viruses can infect humans, such as poultry, pigs, and horses. Influenza B viruses only infect humans; influenza C viruses are prevalent in both humans and pigs. According to the evolution of viral genes, the influenza viruses in all mammals are derived from avian influenza viruses. The genetic evolution rates of different animal influenza viruses are different. The human influenza A virus HA and NA genes have the fastest evolution, and the avian influenza virus is slower.

Vaccination
The flu virus is highly contagious and spreads quickly, which is easy to cause a pandemic. In addition to strengthening the physical exercise to enhance physical fitness, to maintain room hygiene, to avoid crowds during the epidemic, and to perform necessary air disinfection in public places, vaccination can significantly reduce the incidence and alleviate symptoms. However, due to the continual variability of the influenza virus, it is only necessary to master the dynamics of influenza virus mutations, and to select new epidemic strains in order to prepare a vaccine with specific preventive effects in time. The vaccines used are inactivated vaccines and live attenuated vaccines. It has been reported that a live attenuated vaccine on the market is a vaccine strain produced by crossing a temperature-sensitive attenuated strain (Ca) A AnnArbor/6/60 (H2N2) with a wild strain of H1N1 or H3N2.
The advantage of inactivated vaccine is that it can produce a large amount of IgG by subcutaneous injection, and the side effect is small. The disadvantage is that the local sIgA is small and the number of inoculations is large. The live attenuated vaccine is inoculated by nasopharyngeal spray method. Although the operation is simple and convenient, the local SIgA is more, but the side effects are large, similar to mild infection.
The HA and NA subunit vaccines developed have small side effects, inhibiting the replication and spread of the virus in the respiratory tract, and alleviating clinical symptoms. A large number of studies on influenza virus genetic engineering vaccines have been carried out abroad. The HA gene of influenza virus has been recombined into the vaccinia virus gene by genetic recombination method, and a recombinant vaccine has been prepared and expressed. It can be confirmed by animal vaccination to produce specific antibodies.
There is no effective treatment, mainly symptomatic treatment and prevention of secondary bacterial infections.
On June 11, 2018, the tetravalent influenza virus split vaccine was approved for marketing in China to prevent influenza virus infection in people aged 3 years and older. The approved tetravalent influenza virus split vaccine in addition to the common trivalent influenza vaccine. In addition to the A1, A3, and BV viruses, the BY type influenza virus is also included.

Research progress

US researchers say they have found a new anti-influenza drug that can stop those resistant strains from spreading, posing hope for the treatment of the flu. According to a report published in the journal Science, researchers have achieved effective results in experiments on mice. Researchers are currently experimenting with other animals to test their efficacy.
The new drug blocks it from attacking other cells by blocking an important enzyme (neuraminidase) on the surface of the influenza virus. This enzyme links the flu virus to human cells and then infects new cells.
The new anti-influenza drug developed by scientists can permanently attach to the enzyme, block its movement, and then stop the virus from spreading to other cells. Scientists call this new drug DFSAs. Because of the action of drugs, the flu virus can only self-destruct if it wants to continue to move and reproduce, so it can no longer infect other cells.

Important events

Japanese scholars have made the H1N1 super virus approved for madness, and human infection will definitely die.
In July 2014, in order to analyze the genetic changes of the influenza virus H1N1, Professor Hegang Yoshihiro of the University of Tokyo and the University of Madison, Wisconsin, developed a new variant. The variant H1N1 can bypass the human immune system and is considered to be Super virus. Once this life-threatening virus is leaked out, human beings will have no resistance and may become a huge disaster. He Gang said that he has indeed developed this super flu virus. He stated that the preliminary research report had been submitted to the World Health Organization Committee and received favorable comments.
However, there are still many scientists who are cautious about this. Some scientists believe that Hegang has extracted the virus from the virus strain and made a super virus. This is too crazy.
US scientists make a deadly flu virus controversy can cause a pandemic
On June 11, 2014, American scientists said they used the flu gene fragments that are being spread in wild ducks to create a deadly virus that is extremely similar to the "Spanish flu" virus. Although the researchers believe that this outcome will help deal with the next influenza pandemic, this experiment is still criticized by some as "recklessness," "crazy," and "dangerous." The head of the experiment is Hegang Yiyu, a professor of virology at the University of Wisconsin-Madison. In 2011, he and the Dutch medical scientist Ron Fuhiye studied how the transmission of the H5N1 avian influenza virus would be enhanced, but its experiment. The method has been criticized. Later, the relevant experiment was suspended for one year and was not restarted until 2013.
Experiments using ferrets have shown that the new virus is more pathogenic than the normal avian flu virus, but lower than the "Spanish flu" virus and cannot be spread by droplets. The ferrets are often used to test for the effects of influenza viruses because of their characteristics similar to humans. As long as the 7 amino acids of some of the key proteins of the above new virus are mutated, their ability to spread will be significantly improved, and the ferrets can be easily transmitted through the air. Researchers believe that the new virus has the potential to cause a pandemic in the population.
Professor Robert May, former chairman of the Royal Society, still told the media that the work was “completely crazy” and that the whole incident was “extremely dangerous”. Harvard professor Mark Lipsic also expressed concern: “Even in the safest laboratories, this is a dangerous act. Scientists should not take such risks unless there is strong evidence that their work can save lives. However, their papers did not provide. There is a view that the H1N1 flu virus that caused many people to die or even die is caused by a laboratory accident.

No comments:

Post a Comment