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:
- Herpesviridae: Herpes simplex 1 & 2 Varicella Zoster virus
- Herpesviridae: Cytomegalovirus & HHV 6 & 7
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:

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 its antigenic makeup, and by its 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)

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.

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)

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

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

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

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

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 bodys 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 bakers 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 1545% of infected persons spontaneously clear
The remaining 5585% 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

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.

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

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

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.