Virology summary

VIROLOGY  General characteristics  Acellular  Ultramicroscopic  Obligate intracellular parasites  Unable to replicate (multiply) on their own  Lack the genes and enzymes  Depend on the ribosomes, enzymes, and metabolites  Filterable  Virus and bacteria table for comparison

 Host range is determined by – “viruses ability to interact with host cell  Binding sites on viral capsid or envelope combine with receptor sites on host cell membrane  Made up of two parts

1. Nucleic acid 2. Capsid (protein coat) [composed of many small protein units called capsomeres]  Nucleic acid + capsid = the nucleocapsid  Some capsids are surrounded by envelope  Virions are complete, fully developed viral particles composed of nucleic acid surrounded by a coat.  Three types 1- Helical 2- Polyhedral 3- Complex  VIRAL CAPSID: composed of small protein subunits called capsomers. The arrangement of the capsomers determines virus symmetry. 1. 2. 3. 4.

FUNCTIONS : It protects the viral genome It is responsible for the structural symmetry of the virions It participates in attachment of the virions to susceptible cells Capsid proteins are important antigens. (immunity)

 Basic structural forms 1. Naked icosahedral [e.g. poliovirus, adenovirus, hepatitis A virus] 2. Naked helical [e.g. tobacco mosaic virus ] 3. Enveloped icosahedral [e.g. herpes virus, yellow fever virus, rubella virus] 4. Enveloped helical [e.g. rabies virus, influenza virus, parainfluenza virus, mumps virus, measles virus] 5. Complex [e.g. poxvirus] NOTE: read slides 43 – 49 [ virus affecting specific systems ]

 Bacteriophage : Viruses that use bacterial cell as a host - Area of lyses called a plaque on the surface of the agar.  Titer: concentration of the virus in the suspension  Three methods used for culturing animal viruses: 1. Living animal 2. Embryonated eggs 3. Cell culture 

Specimens are are mostly contaminated 1. Stool 2. Sputum 3. Urine

LEC 2  Western blot : identification of antibodies in patient serum.  Negri bodies : Found in rabies infection.  Cytomegalic intutioin bodies: found in CMV infection.

 Rota virus and Adeno virus, sample is taken from stool.  HSV, VZV, sample is taken from vesicle fluid  Papiloma virus, sample is taken from skin scrapings

VIRUS SEROLOGY:  Used to confirm the diagnosis when the virus cannot be cultivated. We use IgM, but is undetectable 1-4 months after acute infection resolves Criteria for diagnosing primary infection. -Presence of igm and sero conversion. Criteria for diagnosing re infection -Absence or slight increase in IgM -Extremely high IgG.

VIRAL HEMAGGLUTINATOIN:  Idea of test : works without antigen antibody reaction, so its natural. Main function is to detect the presence of viral particles. The test does not discriminate between viral particles that are infectious and particles that are degraded and no longer able to infect cells.  Viruses that can be detected this way : Mumps, measles and influenza  Influenza has viral hemagglutinatin protein. This binds to receptors on RBC surface on sialic acid.  Very sensitive and can detect very small amount of antigen

NEUTRALISATION REACTIONS  Is an antigen antibody reaction that involves formation of specific antibodies ( called antitoxins) to neutralize the harmful effect on bacterial exotoxins.

COMPLEMENT FIXATION REACTIONS

 Complements are a group of serum proteins that bind to antigen antibody complex, they are either used up or fixed..  If they are fixed : Complement fixation reactions.  They are based on depletion of a fixed amount of complement in the presence of antigen antibody reaction. Useful in two conditions 1: Very small amounts of antibody 2: when amount of antibody is too low to cause precipitation or hemagglutination reactions. Now a days it is used for diagnosis of viral, fungal and rickettsia diseases FLORESCENT ANTIBODY TECHNIQUES ( LABLED REACTIONS ) To identify of antigens in clinical specimens or detect the presence of specific antibody in serum. The procedure is quick, sensitive, and very specific. They use antibodies labeled with florescent dyes ( isothiocynate ) to visualize them under UV light. Florescent antibody test are two types: 1: Direct florescent antibody test Eg: rabies virus ( LYSSA VIRUS ) (rhabdo virus family) 2: indirect florescent antibody test Eg: identification of tripoima palladium ENZYME LINKED IMMMUNO SORBANT ESSAY (ELISA) IDEA: Use antibodies linked to an enzyme. The enzyme is use to detect antigen antibody reactions.substrate is added to determine if the enzyme is linked to antibody. If yes the substrate is conmverted to a product that causes a colour change. Enzymes used 1: horse radish perixodase\ 2: alkaline phosphatase. Two basic methods 1: direct ELISA: for detection of antigens 2: indirect ELISA: for detection of antibodies.

VIRAL IDENTIFICATION BY MOLECULAR METHODS They require 2-6 hrs.two types

1: Nucleic acid detection.: uses nuclic acid probes – short segments of DNA complementary to viral DNA or RNA. Best used when the amount of virus used is abundant. EG: Papilloma virus in cervical cells. 2: Nucleic acid amplification (pcr): used for amplification of short sequence of a target DNA or RNA

Lec 3 DOUBLE STRANDED ENVELOPED DNA VIRUS  General  Herpes viruses : - Have the ability to establish latent infection.       

Simplexvirus (HHV1 and HHV 2), (HSV) type 1 & type2 Varicella –Zoster virus (HHV 3) Epstein-Barr virus (HHV 4) Cytomegalovirus (HHV 5) Roseolovirus (HHV 6), (SIX DISEASE) HHV 7 (T-lymphotropic virus) Kaposi's sarcoma (HHV 8)

 Subfamilies:  α- Herpesviridae: Herpes simplex 1 & 2 Varicella –Zoster virus  β- Herpesviridae: Cytomegalovirus & HHV 6 & 7  δ Herpesviridae: Epstein-Barr virus & HHV 8  Herpes Viruses Morphology:

    

Double strand DNA Icosahedral Nucleocapsid is surrounded by a lipid envelop derived from cell membrane Contain glycoprotein spikes. Replication and assembly of capsid takes place within the nucleus

 Recurrence can be triggered by:

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Exposure to ultraviolet radiation Emotional upset Hormonal change associated with menstruation Heat Fever

HERPES VIRUSES HSV-1 • Mainly transmitted by contact with the HSV-1 virus found in cold sores, saliva, and surfaces in or around the mouth and lips. • Also be transmitted through oral sex to cause genital herpes. • Those affected by HSV-1 are unlikely to be affected by HSV-2 in the genital area. • Mostly occur during childhood. Infection is lifelong. • NOTE: A person with herpes dosent have to have symptoms to spread the virus to someone else. • Infection: usually in infancy.  ORAL FACIAL HERPES:1: Acute gingivistomatitis: most common manifestation of primary herpetic

infection. • Pain and bleeding in gums. • Ulcers with necrotic base present. • Enlarged neck glands. • Self limiting that lasts 13 days. 2: Herpes labialis (cold sore): following primary infection, 45% experiences

reactivation. • Is a recurrence of oral HSV.  SKIN INFECTION:-

• Herpetic whitlow: HSV-1 can be transmitted by skin contact  EYE INFECTION:-

• Herpetic Keratitis • Is an infection of the cornea, often result in deep ulcers

 HERPES ENCEPHALITIS:-

• HSV-2 could be more serious • Virus may reach the brain during viraemia • Olfactory tract and Trigeminal ganglia affected.

HERPES VIRUSES HSV-2 • Differentiated from HSV-1 by it’s antigenic makeup, and by it’s effect on cells in tissue culture, serology (anti -2 antibodies), PCR. • Latent in the sacral nerve ganglia found near the base of the spine. • Transmitted primarily by sexual contact • Cause genital herpes • Often has no symptoms, or mild symptoms that go unrecognized • Incubation is one week • Pregnant women who have genital herpes can transmit hsv-2 or hsv-1 to their infant, through contact with the virus during delivery. • The lesions of genital herpes are particularly prone to secondary bacterial infection eg. S.aureus, streptococcus, trichomonas and candida albicans. • Dysuria is a common complaint, in severe cases, there may be urinary retention. • Vesicles contain infectious fluid. • Semen may contain the virus. • The virus enters a lifelong latent state in nerve cells.

NEONATAL HERPES SIMPLEX (1) • The baby is usually infected perinatally during passage through the birth canal. • Premature rupturing of the membranes is a major risk factor. • The risk of perinatal transmission is greatest when there is a florid primary infection in the mother. • Smaller risk from recurrent lesions in the mother, probably because of the lower viral load and the presence of specific antibody

NEONATAL HERPES SIMPLEX (2)

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The virus can cross the placental barrier and affect the fetus. Spontaneous abortion or serious fetal damage Particularly dangerous in premature infants HSV infection varies from a mild disease localized to the skin to a fatal disseminated infection.Organs most commonly involved are the liver, adrenals and the brain.

• Brain is involved, the prognosis is particularly severe. The encephalitis is global and of such severity that the brain may be liquefied. • Survivors of neonatal HSV infection have residual disabilities. • Acyclovir should be promptly given in all suspected cases • Prevention :- Caesarean section to mothers with florid genital HSV lesions. 

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DIAGNOSIS:• Laboratory Diagnosis • Specimen: vesicular fluid, swab from base of the ulcer. • Electron microscope • Immunofluorescence of skin scrapings - can distinguish between HSV and VZV • Virus isolation • Serology • ELISA • PCR PREVENTION:• Should abstain from sexual activity whilst experiencing symptoms of genital herpes • Hsv-2 is most contagious during an outbreak of sores, but can also be transmitted when no symptoms are felt or visible. • Use of condoms • Medical male circumcision can provide men life-long partial protection against hsv, hiv, and human papillomavirus (hpv)

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TREATMENT:• Antivirals, such as acyclovir, famciclovir, and valacyclovir are the most effective medications • help to reduce the severity and frequency of symptoms but they cannot cure the infection.

VARICELLA ZOSTER CHICKENPOX (VARICELLA) & SHINGLES (HERPES ZOSTER) • Infection with vzv presents in two forms • The primary infection varicella (chickenpox), is a generalized eruption. • The reactivated infection zoster (shingles) is localized to one or few dermatomas • Most common in childhood, highest prevalence occurring in the 4 - 10 years old age group. • Highly communicable  VARICELLA ( CHICKENPOX ) • Varicella-virus is transmitted by the respiratory route and is localized in skin cells, causing a vesicular rash 3-4 days. • Is a primary infection • Incubation 18-21 days • Cause chickenpox. • The virus then moved to the dorsal root ganglion near the spine, where it remains latent indefinitely. • The disease is usually mild • Complications include encephalitis, pneumonia, and Reye's syndrome. • Later , usually in late adulthood, the latent virus becomes reactivated, causing shingles. • Reactivation can be caused by stress or weakening of the immune system  SHINGLES (HERPES ZOSTER) • • • • •

Secondary infection. Transmission, re-infection, re-activation Virus can remain latent in nerve cells and subsequently activate as shingles. Characterized by Vesicular rash along the affected cutaneous sensory nerves, (intercostal, trigeminal

• Band of rose or band of hell • Very painful • Treated with Acyclovir AND An attenuated live vaccine is available

 CONGENITAL VZV INFECTION • Most pregnant women already immune so primary infection is rare during pregnancy. • Primary infection during pregnancy carries a greater risk of severe disease, in particular pneumonia. • Mostly occurs during the first 20 weeks of Pregnancy Clinical signs: • Scarring of skin • Hypoplasia of limbs • CNS and eye defects • Death in infancy normal  NEONATAL VARICELLA • VZV can cross the placenta in the late stages of pregnancy to infect the fetus congenitally • Vary from a mild disease to a fatal disseminated infection. • If rash in mother occurs more than 1 week before delivery, then sufficient immunity would have been transferred to the fetus. • Zoster immunoglobulin should be given to susceptible pregnant women • Zoster immunoglobulin should also be given to infants whose mothers develop varicella during the last 7 days of pregnancy or the first 14 days after delivery  LABORATORY DIAGNOSIS • Clinical presentations are so characteristic that laboratory confirmation is rarely required. • Laboratory diagnosis is required only for atypical presentations, particularly in the immunocompromised. • Virus isolation: requires 2-3 weeks for a results. • Direct detection: electron microscopy may be used for vesicle fluids but cannot distinguish between HSV and VZV • Immunofluorescence: On skin scrappings can distinguish between the two. • Serology: The presence of VZV IgG is indicative of past infection and immunity. • The presence of IgM is indicative of recent primary infection.

Lec 5 HEPATITIS • •

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5 different viruses = Hepatitis A, B, C, D, & E

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Hepatitis may result from infection with other viruses, Epstein-Barr virus (EBV), and cytomegalovirus (CMV).

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Symptoms include loss of appetite, malaise, fever, and jaundice.

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HEPATITIS A

 Hepatitis A virus is the causative agent  HAV=Picornaviruses family, non envelope, ss -RNA icosahedra virus, it can be grown in cell culture.  HAV is able to survive the body’s highly acidic digestive tract and can live outside the body for months.  High temperatures kill the virus, although freezing temperatures do not. Its resistant to chlorine disinfectants.  Oysters are also a source of infection  HAV can survive for several days on surfaces (cutting boards.)  Transmission: from subclinical infected persons  the initial symptoms are : Anorexia,, nausea , diarrhea ,abdominal discomfort, fever, chills and in some cases there is also jaundice ,dark urine and clay-colored stool.  No chronic Hepatitis A.  HAV may be shed in feces for 10 days before clinical symptoms appear.  the virus is not linked to liver cancer.  Diagnosis is based on tests for IgM antibodies, (ELISA) They appear about 4 weeks after infection  Recovery results in lifelong Immunity  Transmission : Oro-fecal HEPATITIS  Diagnosis: Three serologic markers available: 1. Hepatitis A Total (IgG and IgM) antibody 2. Hepatitis A IgM 3. Hepatitis A IgG  Detecting IgM anti-HAV in the serum of a patient  Liver biopsy is not indicated  Testing for anti-HAV IgG is not helpful in the diagnosis  HAV antigen can be detected in the stool or body fluids  Treatment: HAV – no specific treatment as it will often resolve itself spontaneously  Passive immunization (immunoglobulin) can provide temporary protection  All HAV vaccines contain inactivated (killed) virus = HAVRIX  Havrix is recommended as 2 injections 6-12 months apart Hepatitis B

 Hepatitis B (Serum Hepatitis)  Hepatitis B virus (HBV) is the causative agent of hepatitis. HBV is classified as  hepadna virus.  HBV is large double-strand DNA envelope virus.  It passes through an intermediate RNA stage using viral reverse transcriptase resembling retrovirus.(HBV uses reverse transcriptase to produce its DNA from m RNA)  Hepatitis B virus can survive outside the body at least 7 days  Transmitted by blood, and body fluids.  The serum from patient with HBV contain three distinct particles: 1- Dane particles (largest) is the complete virion, it is infectious and capable of replicating. o 2- Spherical particles (smaller). [enveloped particle] o 3- Filamentous particles (tubular enveloped particle] o

 Spherical & filamentous particles are unassembled component without nucleic acid, (non-infectious). They contain hepatitis B surface antigen (HBSAg),{envelope}.  The antibody tests make convenient screening of blood for HBV.  Transmission : by contaminated syringes, and semen (donated for artificial insemination).  HBV is not spread through food or water, sharing eating utensils, breastfeeding, hugging, kissing, hand holding, coughing, or sneezing  HBV is transmitted by blood transfusions through sharing of razors and toothbrushes.  Intravenous drug users. Blood may contain billion viruses per/ milliliter. (body fluids)  Mothers positive for (HBSAg), may transmit the disease to her infant, usually at birth  After entering the blood the virus infect hepatocytes (specific receptors).  The average incubation period is 3 months  recovery is usually complete, but some patients develop a chronic infection or become carriers.  If (HBSAg), persist for more than about 6 months , it is an indication of chronic HBV hepatitis  Loss of appetite, fever, joint pains and jaundice.  Clinically can not be distinguished from other viral hepatitis

 90% of the acute end in complete recovery.  10% become chronic carriers of HBV.  Approximately 90% of infected infants will develop chronic infection.  25-50 % in children  Diagnosis , detection of hepatitis markers antigens, (Ag) and antibodies in the blood by ELISA.  Carriers are reservoir for transmission of the virus, and they also have a high rate of liver diseases.  Liver cancer / chronic HBV infection.  Chronic carriers are 200 times more likely to develop liver cancer Serological testing:  Hepatitis B surface antigen (HBsAg): can be detected in the serum  HBsAg is present in serum during acute infections and persists in chronic infections.  The presence of HBsAg indicates that the person is potentially infectious.  HBsAg is the antigen used to make hepatitis B vaccine.  HBcAg is not detected in the blood. It is detected only in the nuclei of liver cell  HBeAg appears during I.P. shortly after appearance of HBsAg. Its presence indicates that person is highly infectious  Hepatitis B serologic testing involves measurement of several hepatitis B virus (HBV)-specific antigens and antibodies.   Lab diagnosis

• 2- Anti (HBe) • Begins to rise at end of acute stage, appears after anti-HBc and its presence correlates to a decreased infectivity • 3-Antibody to HBsAg (anti-HBs) - resolve acute HBV infection = indicates immunity.  The persistence of HBsAg for 6 months after the diagnosis of acute HBV is indicative of progression to chronic HBV infection}.  Anti - HBc (Antibody to HBV core antigen):  Total - indicates past or active infection; present whether person is immune or chronic carrier  No antigen test  HBeAg (Hepatitis Be antigen):  indicates person is highly infectious  Anti-HBe (Antibody to HBVe antigen):  prognostic for resolution of infection; less infectious    

Acute patients = rest. Chronic patients may be given interferon Viral DNA polymerase inhibitors or pegylated alpha interferon. PEG : (polyethylene glycol) to make interferon last long in the body HBV INFECTION REMAIN NOT CURED

 Liver transplantation is often a final option in treatment.  Prevention 1-Precautions. 2-Screening of blood. 3- Vaccine against HBsAg is available.  A recombinant subunit vaccine has been made for the hepatitis B virus. Scientists inserted hepatitis B genes that code for important antigens into common baker’s yeast.

HEPATITIS C:  Hepatitis C virus (HCV) is a member of Flaviviridae family Single stranded RNA virus, enveloped.  (HCV) is transmitted via blood, or body fluids.  Sharing needles IDU (80% ) infected with HCV.  appearance of detectable HCV antibodies takes 70-80 days  The virus does not kill the cell , but immune reaction can damage the liver cell.  Six different genotypes (genetic variation), besides it is difficult to be cultured  Hepatitis (HCV) causes both acute and chronic infection. Acute HCV infection is usually asymptomatic,  About 15–45% of infected persons spontaneously clear  The remaining 55–85% of persons will develop chronic  chronic HCV infection, the risk of cirrhosis or cancer  Symptoms may take 20 years to appear.  HCV can survive outside the body at room temp. for up to 3 weeks  Diagnosis of hepatitis is made by biochemical assessment of liver function  HCV infection is diagnosed serologically in 2 steps:  Screening for anti-HCV antibodies with a serological test identifies people who have been infected with the virus.  If the test is positive for anti-HCV antibodies  needed to confirm chronic HCV infection  After a person has been diagnosed with chronic hepatitis C infection, they should have an assessment of the degree of liver damage (fibrosis and cirrhosis).  Treatment: Interferon & ribavirin.( Guanine inhibitor)  oral directly acting antiviral agent (DAAs) therapies (targeted against viral protein, (protease)  major reason for Liver transplantation  Prevention  minimizing exposure to sharing of items such as razors, toothbrushes, & nail clippers.  Person with HCV should be vaccinated against HAV,HBV (Twinrix). Havrix is a HAV vaccine.

 Having had hepatitis C once does not make you "immune" from getting hepatitis C again  No vaccine   

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HEPATITIS D  Hepatitis D virus (HDV).  discover in carriers of HBV.  Hepatitis D virus (HDV) has a circular single strand of RNA, and is not able to cause an infection.  It becomes infectious when an external envelop HBsAg,(HBV) whose formation is controlled by the genome of HBV , cover the HDV protein core (the delta antigen).  Can only infect individuals with HBV.  Transmission is via blood or body fluids  Can occur as either acute (coinfection form) or  chronic (superinfection form).

 In chronic HBV, chronic HDV was often  accompanied by progressive liver damage

HEPATITIS E  Hepatitis E virus (HEV).  Calciviridae.  Non-enveloped single strand RNA virus.  Similar to HAV, but not related serologically.  Hepatitis E virus (HEV) is spread by the fecal oral route.  Does not cause chronic liver disease. Hepatitis G (HGV) 1) Similar to HCV 2) About 20% of HCV patients have HGV 3) Is more prevalent than HCV. • Molecular assays o Commercial assays for HBV DNA and HCV RNA (must be separated from cells) o In-house assays for HAV RNA & HDV RNA o No molecular assay for HEV RNA Lec 6:

Viral Diseases of the Respiratory System 1. Influenza v. 2. Parainfluenza v.     

Ciliary escalator of the lower respiratory keeps it STERILE ! Microbes in the lungs can be phagocytized by alveolar macrophages. Respiratory mucus contains IgA antibodies Common cold is cause by : Rhinovirus or Coronavirus Rhinovirus = Picornaviridae, single-strand RNA, non-enveloped virus. Grow best slightly below body temperature.  A sever complication of bronchitis is pneumonia  Viral pneumonia occurs as a complication of influenza, measles, or chickenpox.

Respiratory Synctial Virus:        

Paramyxovirus The most common viral respiratory disease in infants; 4,500 deaths annually. Causes cell fusion (syncytium) in cell culture Symptoms: Pneumonia in infants Sample nasopharyngeal swab/wash Diagnosis: Serological test for viruses and antibodies. CPE in C.C, E.M No haemagglutinin, No heamolysin, No growth in E.E Treatment: Ribavirin.

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Influenza virus Influenza viruses are members of the family Orthomyxoviridae. Three types of influenza virus are known; A, B & C Influenza. A- causes worldwide Influenza epidemics every 10-12 years (pandemics) and outbreaks every year. B- causes outbreaks, but less often than A. C- cause mild R.D. The influenza virus is an infectious disease of birds and mammals caused by RNA viruses. Commonly confused with a cold, the flu is a much more severe disease. incubation time of 2-3 days. mortality, very young and very old

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 Illness

 Influenza

 Common cold

 Clinical spectrum

 Often systemic

 Mostly local

 Speed of onset

 Abrupt

 Gradual

 Fever

 Usually high

 Usually low-grade

 Presentation

 Chills, , malaise, sore throat

 Sneezing, sore throat, nasal congestion

 Fatigue

 Marked

 Mild

 Course

 Unwell for 1-2 weeks, chest problems common, severe malaise

 Rapid recovery

 Complications

 More common and often severe pneumonia

 Uncommon

 Occurrence

 Seasonal

 All year round

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numerous projections that characterize the virus. (Spikes) There are two types of projections: Hemagglutinin (HA) spikes. Neuraminidase (NA) spikes.  Helical nucleocapsid  Haemagglutinin  about 500 on each virus  allow the virus to:  Recognize, and attach to body cells  HA binds to cell surface receptor (sialic  acid) to initiate infection  responsible for pathogenicity of the  virus).  Main determinant of immunity.  Neuraminidase  about 100 per virus  allow the virus to:  Separate from the infected cell as the virus exit after  intracellular reproduction.  Shift (only for influenza A).  Drift (both influenza A and B)  Viral strains are identified by variation in HA & NA antigens.  Change in HA and NA determine the antigenicity of the virus.  Influenza A- virus ared found circulating in birds, human, swine & horses  antigenic shifts: Each number change represents a substantial alteration in the protein makeup of the spike.  Antigenic shifts are probably caused by: Major genetic recombination  Recombination is likely in infections caused by more than one strain.  genetic change process is called Reassortment.  Swine is a good mixing vessels in which recombination, reassortment can occur.  Antigenic shift: Probably due to genetic recombination between different strains infecting the same cell.  Changes in HA and NA spikes so is the cause of recurring epidemics  Antigenic shift, however, occurs only in influenza virus A because it infects more than just humans.

 Virus strains preferentially bind to sialic acids alpha (2,3) linkage. This is the major sialic acid on epithelial cells of the duck gut.  major type of sialic acid present on human respiratory epithelial cells.  efficient human to human transmission requires that the avian viruses recognize sialic acids with alpha(2,6) linkages.  Epithelial cells of the pig trachea produce both alpha(2,3) and alpha(2,6) linked sialic acids. This is believed to be the reason why pigs can be infected with both avian and human  Global herd immunity to the new virus is usually very low and this can result in a new flu pandemic.  This phenomenon only occurs with influenza A.  Only H1, 2 and 3 and N1 and N2 subtypes circulate widely in human.  Epidemic: human-to-human spread of the virus into at least two countries in one WHO region  Pandemic: human-to-human spread of the virus with community level outbreaks in at least one other country in a different WHO region than initial epidemic.

 Drift (minor antigenic change) change their antigenic character gradually over time. i. This is due to random point mutations introduced ii. during replication of the viral genome. iii. Drift results in annual epidemics of influenza A and B in humans. Influenza viruses are also classified into groups according to the antigens in their protein coat Influenza A  Highly infective  Infects many species  Causes widespread epidemics Influenza B  Found only in humans  Milder infections  Regional epidemics Influenza C  Causes mild disease  Does not cause epidemics  Samples : Oropharyngeal (Throat) + Nasopharyngeal Swab  Amantadine and Rimantadine Are effective against influenza A viruses but NOT against influenza B viruses. The mechanism of amantadine's antiviral activity involves interference with the viral protein M2

Influenza B structurally distinct M2 channels which is responsible for the ineffectiveness of this drug.  Neuraminidase inhibitors : Are a class of drugs which block the neuraminidase enzyme. Tamiflu, Relenza belong to this class neuraminidase inhibitors act against both influenza A and influenza  Parainfluenza virus:  Paramyxovirus: Pleomorphic, enveloped ssRNA viruses. There are two types of glycoprotein in the envelope, namely the HN (haemagglutinin / neuraminidase) and the F (Fusion).  Haemagglutinin binds, agglutinates RBCs.  Neuraminidase enzyme that degrades sialic acid (detaches the virion from the cell surface)  Humans are the only host (any age)  Diagnosis: Lab, serology & tissue culture  Treatment: Symptomatic , & no vaccine.