RNA enveloped viruses Influenza viruses

1. RNA Enveloped
Viruses
Dr Mohammed Salah 1
LECTURE III

2. DNA containing
viruses
Viruses
RNA containing
viruses
Enveloped Non-enveloped
(Naked)
Enveloped Non-enveloped
(Naked)

3. Enveloped RNA Containing Viruses
1. Orthomyxoviruses [segmented nucleic acid (7 - 8 segments)]
A. Influenza A, B and C viruses.
B. Avian influenza virus.
C. Swine influenza virus.
2. Paramyxoviruses (non-segmented nucleic acid)
A. Para-influenza viruses.
B. Mumps virus.
C. Measles virus.
D. Respiratory syncytial virus.

4. 3. Togaviruses;
 Rubella (German measles) virus.
5. Rhabdoviruses;
 Rabies virus.
6. Retroviruses;
 Human immunodeficiency viruses (HIV).
4. Flaviviruses;
 Yellow fever virus.
7. Coronaviruses;
 SARS-CoV-1 and SARS-CoV-2.
Enveloped RNA Containing Viruses

5. 1. Picornaviruses;
Poliovirus
Coxsackie viruses
Echoviruses
2. Reoviruses;
Rotavirus
Acid resistant
Acid resistant
Hepatoviruses
Rhinoviruses Acid sensitive
Hepatitis A virus
Enteroviruses
Non-Enveloped RNA Containing Viruses
Acid resistant

6. I. Orthomyxoviruses
A. Influenza Viruses
Dr Mohammed Salah 6

7. • They are pleomorphic ( spherical or tubular),
enveloped RNA viruses.
• The nucleocapsid is helical with negative
sense SS RNA genome. In case of influenza
A&B the genome consists of 8 segments.
• The envelope is composed of lipid bilayer:
• inner matrix M protein
• outer surface 2 glycoprotein spikes
1-{hemagglutinin (HA)
2- and neuraminidase (NA)},
which are two important antigens.
Dr Mohammed Salah 7
1) Viral structure

8. 1. Haemagglutinin (H);
♦ Antigenic glycoprotein present on viral surface
♦ responsible for their attachment to specific receptors
on host cells.
Dr Mohammed Salah 8
2. Neuraminidase (N);
♦ Antigenic glycosylated enzyme, present on the surface of influenza viruses;
♦ Cleaves sialic acid residue of the N-acetylneuraminic acid in mucus resulting in their
liquefaction and subsequent viral spreading to the ciliated epithelial cells.
♦ Facilitates the release of viral progeny from infected cells after their budding from the
plasma membrane
 Viral physiological functions of H &N
spikes

9. ►Both Haemagglutinin (H) and neuraminidase (N) are target for
Antiviral drugs and antibodies.
►Antibodies (antigenic); directed against these two surface antigens are
responsible for immunity to infection.
►Variability is responsible for serious epidemics of the disease that
recur in human.
►Used as the basis for the naming of the different subtypes of influenza
A viruses. This is where the H and N come from in case of;
H1N1 (Swine flu) ‫الخنازير‬ ‫انفلوانزا‬
H2N2 (Asian flu) ‫االسيويه‬ ‫االنفلوانزا‬
H5N1 (bird flu) ‫انفلوانزا‬
‫الطيور‬
Dr Mohammed Salah 9
□ Antigenic variation

10.  Common in influenza virus.
 Antigenic Variation
 Resulted from changes in the H (16 types) and N (9 types)
antigens.
 Types;
Antigenic drift:
 Minor changes due to mutation
 Each 1 year
 affects the severity of the disease only, why?
Antigenic shift:
 Major changes due to genetic recombination/ reassortment
between two different strains and results in new antigenic type
which usually starts an epidemic or even pandemic why?

11. □ Classification
1) Influenza type A; contain 8 RNA segments, affect
human and animals and causes severe disease.
2) Influenza type B; contain 8 RNA segments affect
human only with less severity.
3) Influenza type C; contain only 7 RNA segments,
single surface glycoprotein [H-esterase-fusion
protein (HEF)], causes mild RTI and is of relatively
little importance.
 Nucleoprotein antigen (no serologic cross reactivity);
 Stable and classify the influenza virus into 3 types;

12. Dr Mohammed Salah 12
□ Pathogenesis
Transmission: influenza viruses spread mainly through small droplets containing
influenza virus. These droplets are expelled into the air when people infected
with the flu cough, sneeze or talk.

13. oThe viruses transmitted by inhalation through droplet infection by
sneezing and coughing.
oThe inhaled virus lands in the lower respiratory tract (tracheobronchial
tree), and then carried to the lungs [localized infection (no viremia)] .
oHaemagglutinin attaches to specific receptors on ciliated epithelial cells
to which the viral envelope fuses with subsequent entering of viral RNA
into the host cell.
oThe viral envelope neuraminidase enzyme cleaves sialic acid residue of
the N-acetylneuraminic acid in mucus resulting in their liquefaction.
oThese liquefied mucus facilitating viral spreading and their penetration
to mucus secreting and ciliated epithelial cells causing their destruction.
Dr Mohammed Salah 13
□ Pathogenesis

14. Symptoms 1. Nonproductive cough ‫جافه‬ ‫كحه‬, sore throat, and nasal
discharge.‫رشح‬
2. Fever, coryza, malaise, muscle ache, and general
prostration.
3. Complication with secondary bacterial infection
(pneumonia) may occur.
Laboratory
diagnosis:
1. Detection of rising antibody titer by hemagglutination
inhibition, ELISA or RIA.
2. Finger printing for detection of the different
genotypes and strains.
Treatment 1. Salicylates and antihistaminics
2. Amantadine and rimantadine are effective for
prophylaxis and during the first 24 hrs of infection
with influenza type A.
3. Vitamine C and rest in bed.
Prophylaxis: Immunization with formalin killed vaccine are
available each year with the suspected type A and B
variants. Dr Mohammed Salah 14

15.  Common cold and influenza

16.  Annual influenza immunization
Short life immunity to influenza virus is due to
1. Continuous variation (shift and drift) of the virus.
2. The virus rarely invades the blood, if ever.
3. The short incubation period as well as the short disease time
Both are indicated for the prevention of influenza disease caused by the two influenza A virus subtypes and
the two influenza B virus types contained in the vaccine for:
• active immunisation of adults, including pregnant women, and children from 6 months of age and older
• passive protection of infant(s) from birth to less than 6 months of age following vaccination of pregnant
women
People may experience cold and flu-like symptoms for up to 24-48 hours after getting the vaccine. This shows the
body's immune response is kicking in and the vaccine is working.

17.  Influvac subunit tetra vaccine

18.  Vaxigrip Tetra

19. ⁃ Subtype (with the same structure features) of influenza A virus (A/H5N1 virus);
⁃ Cause illness in humans and many other animal species.
⁃ The causative agent of avian flu, avian influenza, or bird flu.
⁃ Transmission:- It believed that these cases resulted from contact with infected birds or
surfaces contaminated with excretions from infected birds.
 Avian Influenza Virus (H5N1)
⁃ Symptoms of bird flu in humans:-The main symptoms of bird flu can appear very
quickly and include:
a) a very high temperature or feeling hot or shivery
b) aching muscles
c) headache
d) a cough or shortness of breath

20. ►Treatment:- The virus resistant to
amantadine and ramantadine (antiviral drugs
commonly used for influenza).
►Oseltamivir (Tamiflu)® and zanamavir
(Relenza)®, Antiviral medicines help
reduce the severity of the condition, prevent
complications and improve the chances of
survival.
►The continual mutation of H5N1 renders
the vaccine of limited use.
►All genes are of bird origin. Human cases
also have been reported.
Dr Mohammed Salah 20
 Avian Influenza Virus (H5N1)
Signs that a bird may be infected with bird flu
include:
•sudden death
•swollen head
•closed and runny eye

21.  Swine Influenza Virus (H1N1)
⁃ Subtype (with the same structure features) of
influenza A virus (A/H1N1 virus); Called H1N1/09
virus;
⁃ Swine origin influenza A virus subtype
H1N1 strain that was responsible for the 2009
swine flu pandemic.
⁃ In pigs, the virus cause swine influenza, swine flu,
pigs influenza, or pigs flu;
⁃ Human normally not get swine flu, but in 2009 a strain of swine flu virus
called H1N1 infected many people around the world causing zoonotic swine
influenza in human.
⁃ These strains of swine flu rarely pass from human to human

22.  Swine Influenza Virus (H1N1)
Transmission Direct contact with infected pigs or contaminated
surfaces.
Airborne through the aerosols produced by pigs
coughing or sneezing.
Clinical
symptoms
Fever, cough, sore throat, body aches, severe
headache, chills, fatigue, and shortness of breath.
Death: Mostly in young children and the elderly
and caused by;
a) Respiratory failure (most common cause).
b) Pneumonia; leading to sepsis.
c) High fever; leading to neurological problems.
d) Excessive vomiting and diarrhea; leading to
dehydration and electrolyte imbalance.

23.  Swine Influenza Virus (H1N1)
Laboratory
diagnosis
1. Nasopharyngeal swab for viral culture.
2. Detection of H1N1 specific antibodies.
3. RT-PCR detection of H1N1 viral specific nucleic acid.
Treatment a) The virus resistant to amantadine and rimantadine
b) Oseltamavir (Tamiflu)® and zanamavir (Relenza)®.
c) Basic supportive care:- hydration, analgesics and cough
suppressant
Prophylaxis a) Prophylaxis with antiviral agents should be considered in
individuals subjected to infections.
b) The continual mutation of H1N1 renders the vaccine of limited
use.

24.  Why are swine ‘mixing vessels'?
“Species barrier theory”
HA binds to various sialic acids depending upon
species specificity and the linkages of these sialic
acids on host surface cells.
Avian influenza viruses bind preferentially to sialic
acid (alpha 2,3) found in birds,
while human viruses bind primarily to another
(alpha2,6).
Essentially, pigs are mixing vessels because their respiratory epithelial cells have the
receptors for both human and avian influenza viruses, which allows for co-infection and
subsequent recombination events. However, humans could very well become ‘mixing
vessels' since the airway epithelial cells in humans contain receptors for that bind to
human influenza viruses and to less extent to avian influenza

25. Enveloped RNA Containing Viruses
1. Orthomyxoviruses [segmented nucleic acid (7 - 8 segments)]
A. Influenza A, B and C viruses.
B. Avian influenza virus.
C. Swine influenza virus.
2. Paramyxoviruses (non-segmented nucleic acid)
A. Para-influenza viruses.
B. Mumps virus.
C. Measles virus.
D. Respiratory syncytial virus.

26. THANK YOU
END OF LECTURE II
Dr Mohammed Salah 26