Influenza virus

Last updated: February 23, 2023

Influenza virus

Paediatrics Sara

Paediatrics Sara

Seizures: Pathology review
Seizures: Clinical
Seizures and epilepsy
Early infantile epileptic encephalopathy (NORD)
Anticonvulsants and anxiolytics: Benzodiazepines
Nonbenzodiazepine anticonvulsants
Febrile seizure
Meningitis
Meningitis, encephalitis and brain abscesses: Clinical
Neonatal meningitis
Neisseria meningitidis
Central nervous system infections: Pathology review
Disorders of consciousness: Clinical
Cerebral palsy
Cerebral circulation
Neurodevelopmental disorders: Clinical
Pediatric brain tumors
Spina bifida
Congenital disorders: Clinical
Developmental milestones: Clinical
Precocious and delayed puberty: Clinical
Constitutional growth delay
Delayed puberty
Learning disability
Neurofibromatosis
ADHD: Information for patients and families (The Primary School)
Disorders of sex chromosomes: Pathology review
Asthma: Clinical
Asthma
Asthma: Information for patients and families (The Primary School)
Respiratory syncytial virus
Influenza virus
Pediatric lower airway conditions: Clinical
Human parainfluenza viruses
Pneumonia
Moraxella catarrhalis
Pneumonia: Pathology review
Knowledge Shot: What over-the-counter medicine works best at kicking the cough of the common cold and bronchitis
Bronchiectasis
Corynebacterium diphtheriae (Diphtheria)
Croup
Pediatric upper airway conditions: Clinical
Clinical Skills: Using a metered-dose inhaler
Bacterial epiglottitis
Congenital pulmonary airway malformation
Upper respiratory tract infection
Neonatal respiratory distress syndrome
Acute respiratory distress syndrome
Acute respiratory distress syndrome: Clinical
Metabolic and respiratory alkalosis: Clinical
Shock: Clinical
Pediatric vomiting: Clinical
Shock
Pediatric allergies: Clinical
Dengue virus
Yellow fever virus
Zika virus
West Nile Virus Infection
Leptospira
Fever of unknown origin: Clinical
Salmonella typhi (typhoid fever)
Salmonella (non-typhoidal)
Salmonellosis
Epstein-Barr virus (Infectious mononucleosis)
Pediatric ear, nose, and throat conditions: Clinical
Lymphomas: Pathology review
Non-Hodgkin lymphoma
Hodgkin lymphoma
Bordetella pertussis (Whooping cough)
Vaccinations: Clinical
Vaccinations
Clostridium tetani (Tetanus)
Kawasaki disease
Kawasaki disease: Clinical
Vasculitis: Clinical
Vasculitis: Pathology review
Pediatric infectious rashes: Clinical
Diarrhea: Clinical
Gastroenteritis
Vibrio cholerae (Cholera)
Rotavirus
Norovirus
Inflammatory bowel disease: Pathology review
Campylobacter jejuni
Listeria monocytogenes
Tropical sprue
Abdominal pain: Clinical
Intussusception
Congenital gastrointestinal disorders: Pathology review
Diverticular disease: Clinical
Bowel obstruction: Clinical
Pediatric gastrointestinal bleeding: Clinical
Malabsorption syndromes: Pathology review
Nephritic and nephrotic syndromes: Clinical
Nephrotic syndromes: Pathology review
Membranoproliferative glomerulonephritis
Lupus nephritis
Nephritic syndromes: Pathology review
Focal segmental glomerulosclerosis (NORD)
Minimal change disease
Membranous nephropathy
Chronic kidney disease: Clinical
Acute kidney injury: Clinical
Horseshoe kidney
Urinary tract infections (UTIs): Nursing process (ADPIE)
Urinary tract infections: Clinical
Urinary tract infections: Pathology review
Lower urinary tract infection
Urinary incontinence: Pathology review
Acute pyelonephritis
Pediatric urological conditions: Clinical
Postoperative evaluation: Clinical
Chronic pyelonephritis
Kidney stones: Clinical
Proteus mirabilis
Posterior urethral valves
Bladder exstrophy
Hydronephrosis
Growth hormone deficiency
Growth and development
Diabetes mellitus: Pathology review
Diabetes mellitus: Clinical
Hyperkalemia: Clinical
Metabolic acidosis
Thyroid nodules and thyroid cancer: Clinical
Thyroid nodules and thyroid cancer: Pathology review
Thyroid cancer
Hashimoto thyroiditis
Thyroid storm
Thyroid hormones
Hypothyroidism and thyroiditis: Clinical
Thyroid eye disease (NORD)
Thyroid and parathyroid gland histology
Anatomy of the thyroid and parathyroid glands
Hyperthyroidism: Clinical
Hyperthyroidism: Pathology review
Hypothyroidism: Pathology review
Hypothyroidism
Adrenal masses: Pathology review
Primary adrenal insufficiency
Adrenal masses and tumors: Clinical
Congenital adrenal hyperplasia
Adrenal cortical carcinoma
Adrenal insufficiency: Pathology review
Adrenal insufficiency: Clinical
Congenital adrenal hyperplasia: Clinical
Eczematous rashes: Clinical
Atopic dermatitis
Contact dermatitis
Seborrhoeic dermatitis
Blistering skin disorders: Clinical
Papulosquamous and inflammatory skin disorders: Pathology review
Papulosquamous skin disorders: Clinical
Benign hyperpigmented skin lesions: Clinical
Vesiculobullous and desquamating skin disorders: Pathology review
Staphylococcus epidermidis
Measles virus
Appendicitis: Clinical
Congenital TORCH infections: Pathology review
Mumps virus
Human herpesvirus 6 (Roseola)
Pityriasis rosea
Human herpesvirus 8 (Kaposi sarcoma)
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Streptococcus pyogenes (Group A Strep)
Rheumatic heart disease
Varicella zoster virus
Vasculitis
Rapidly progressive glomerulonephritis
Anemia: Clinical
Anemia of chronic disease
Chronic leukemia
Leukemias: Pathology review
Leukemia: Clinical
Acute leukemia
Myeloproliferative neoplasms: Clinical
Bone tumors
Pancoast tumor
Nephroblastoma (Wilms tumor)
Pediatric brain tumors: Pathology review
Stevens-Johnson syndrome
Immune thrombocytopenia
Thrombocytopenia: Clinical
Platelet disorders: Pathology review
Extrinsic hemolytic normocytic anemia: Pathology review
Impetigo
Osteogenesis imperfecta
Imperforate anus
Pediatric orthopedic conditions: Clinical
Slipped capital femoral epiphysis
Femoral hernia
Muscular dystrophy
Muscle weakness: Clinical
Congenital heart defects: Clinical
Cyanotic congenital heart defects: Pathology review
Acyanotic congenital heart defects: Pathology review
Valvular heart disease: Clinical
Valvular heart disease: Pathology review
Congenital syphilis
Congenital rubella syndrome
Congenital toxoplasmosis
Infective endocarditis: Clinical
Endocarditis
Endocarditis: Pathology review
Bacillus cereus (Food poisoning)
Streptococcus viridans
Klebsiella pneumoniae
Enterococcus
Restrictive cardiomyopathy
Neonatal jaundice: Clinical
Jaundice
Jaundice: Pathology review
Jaundice: Clinical
Neonatal sepsis
Neonatal ICU conditions: Clinical
Down syndrome (Trisomy 21)
Edwards syndrome (Trisomy 18)
Mucopolysaccharide storage disease type 2 (Hunter syndrome) (NORD)
Rett syndrome
Reye syndrome
Conn syndrome
Marfan syndrome
Brugada syndrome
Dressler syndrome
Anatomy clinical correlates: Thoracic wall
Neonatal hepatitis
Apnea of prematurity
Fragile X syndrome
Newborn management: Clinical
Sudden infant death syndrome
BRUE, ALTE, and SIDS: Clinical
Shaken baby syndrome
Coarctation of the aorta
Tay-Sachs disease (NORD)
Intestinal atresia
Choanal atresia
Autosomal trisomies: Pathology review
Pyloric stenosis
Aqueductal stenosis
Pediatric constipation: Clinical
Pediatric ophthalmological conditions: Clinical
Pediatric bone and joint infections: Clinical
Skin and soft tissue infections: Clinical
Perinatal infections: Clinical
Disorders of amino acid metabolism: Pathology review
Immunodeficiencies: Clinical
Child abuse: Clinical
Sickle cell disease: Clinical
Cystic fibrosis: Clinical
Congenital cytomegalovirus (NORD)
Delirium

Transcript

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Content Reviewers

Influenza, the virus that causes the flu, is one of the most common infectious diseases.

Now, there are three types of influenza that infect humans, called type A, type B, and type C, each one with slightly different genome and proteins.

Influenza belongs to the virus family Orthomyxoviridae - and type A and B have genomes that are made up of eight RNA segments, whereas type C, has a seven-segment RNA genome, with each segment containing a few genes.

Now, type A, the most common type of influenza virus, can be further subdivided based on two of the glycoproteins on its protective envelope surface; H protein, or Hemagglutinin, and N protein, or neuraminidase.

Hemagglutinin and Neuraminidase can vary a bit in their structure, so different versions are identified by a number.

For example, type A subtype H3N2, sometimes just called H3N2, has hemagglutinin number 3 and neuraminidase number 2 on its surface.

H3N2 and H1N1 are the most common type A subtypes to infect humans, but they both also infect various animals.

To give the full name of a virus, we use the type, the original host that it came from, the location where the virus was first identified, which is usually a city, the strain number, the year of origin, and—for type A influenza—the subtype named by the H and N glycoproteins.

For example, an H1N1 type A flu virus of duck origin from the province of Alberta, Canada, that is the 35th strain discovered in 1976 would be called A/duck/Alberta/35/76 (H1N1).

Type B influenza is less common, it only infects humans and doesn't mutate as often as type A.

Type B influenza only has a few types of H and N glycoproteins on its surface.

Therefore the naming pattern is similar to type A influenza without the H and N subtype included at the end or the host type, since it only infects humans.

For example, a type B virus found in Yamagata, Japan, which is the 16th strain discovered in 1988 would be called B/Yamagata/16/88.

Finally, there's type C influenza which is only one species, and is the least common and least likely to mutate of the three.

Influenza C usually causes mild disease in children, and unlike type B, it can affect both humans and pigs.

Rather than hemagglutinin and neuraminidase, type C influenza uses a hemagglutinin-esterase-fusion protein to enter and exit cells.

So, type C influenza is named without the HN subtype, similar to how type B's written.

For example, a type C virus found in Sao Paulo, Brazil which is the 37th strain discovered in 1982 would be called C/Sao Paulo/37/82.

Of the three types, type A is the most common and causes the most severe illness.

One reason is that the virus has a tendency to mutate its H and N glycoproteins during replication, and this allows daughter viruses to form that are slightly different from one another and from the parent virus.

Over time, if enough of these small changes happen, even if somebody's immune to the original virus, the mutated virus may have H and N glycoproteins that are different enough to allow it to evade antibodies, and therefore infect people who were immune to previous strains.

This process is called genetic drift, and is why individuals can get sick from influenza year after year or from two different strains of influenza in the same year.

In addition, a process called antigenic shift, is where sometimes a virus will be circulating among animal populations like pigs or chickens and then will suddenly change in a way that allows the virus to infect humans as well.

This happens when the same cell, let's say a pig cell, gets infected with two similar flu viruses, for example a flu strain that usually infects humans and one that usually infects pigs.

Since the viral genome is in segments of RNA, the pieces might reassort, or mix, allowing new viruses to have a mix of RNA segments in them.

Reassortment results in viruses that have entirely new hemagglutinin, neuraminidase, or both.

When a virus is produced that can infect human cells and has entirely new proteins, people have little or no protection against it, and it can rapidly spread through the population.

This antigenic shift process is responsible for three major influenza pandemics in the 20th century, including the Spanish Flu in 1918, which killed 3 percent of the world's entire population at the time.

The flu is transmitted when an infected person sneezes or coughs, which spreads thousands of droplets containing the virus into the local area, up to about two meters or six feet away.

These droplets can then land in the mouths or noses of people nearby, or get inhaled into the lungs.

The virus can also survive on surfaces for a few hours, so it's possible to get the virus by touching a surface, like a contaminated doorknob, and then touching your own eyes, nose, or mouth.

When the flu virus enters the body, it uses hemagglutinin to bind to sialic acid sugars on the surface of epithelial cells in the upper respiratory tract.

Once bound, the cell swallows up the virus in a process called endocytosis.

That viral RNA is negative-sense, meaning that each piece first has to be transcribed by RNA polymerase into positive-sense mRNA strands, before it can be translated into proteins and assembled into viruses.

These viruses leave the cell by simply budding out from it by using the neuraminidase, which cleaves the sialic acid sugars in the membrane, releasing the newly created viruses from the cell.

Influenza symptoms start 1-4 days after infection and include fever, headache, runny nose, sore throat, and a cough.

Most of these symptoms get better in a week, but the cough often persists for up to two weeks.

There can sometimes be complications, though, like acute otitis media, bronchiolitis, croup, sinusitis, and pneumonia, including antibiotic-resistant strains caused by Staphylococcus aureus and Streptococcus pneumoniae.

The highest risk of complications is among high-risk groups like young children under 6 months of age, pregnant women, adults over 65 years old, and those with chronic medical conditions, like chronic heart or lung disease.