2. Viruses
Noncellular genetic elements that use a living
cell for their replication and have an
extracellular state.Outside host cell, virus is
known as a virion.
Viruses vary considerably in size (0.02 μm -
0.3 μm) and shape.Smallpox viruses are
among the largest viruses; polio viruses are
among the smallest.
3. Viral structure
Certain viruses contain RNA while other
viruses have DNA
The nucleic acid portion of viruses is known
as genome.
The genome of virus is surrounded by a
protein coat known as a capsid which is
formed from a number of individual protein
molecules called capsomeres.
4. Capsomeres are arranged in a precise and
highly repetitive pattern around nucleic acid.
The combination of genome and capsid is
called nucleocapsid.
5. Classification
Based on morphology
1)Icosahedral
The icosahedron is made up of equilateral
triangles fused together in a spherical shape.
The genetic material is fully enclosed inside
capsid.
Examples of viruses with an icosahedral
structure are poliovirus, rhinovirus, and
adenovirus
6.
7. 2)Helical
virus has its capsid shaped into a rod-shaped
structure. This type of shape has a central
cavity that encloses its nucleic acid.
An example is the tobacco mosaic virus.
8.
9. 3)Complex
Have a combination of icosahedral and helical
shape and may have a complex outer wall or
head-tail morphology.
The head-tail morphology structure is unique
to viruses that only infect bacteria and are
known as bacteriophages. The head of the
virus has an icosahedral shape with a helical
shaped tail.
An example is Poxvirus
10.
11. 4)Enveloped
This virus structure is a conventional
icosahedral or helical structure that is
surrounded by a lipid bilayer membrane,
meaning virus is encased or enveloped.
Examples are Influenza virus, Hepatitis C and
HIV
12.
13. Based on genome replication
The Baltimore Classification System
Class I viruses, double-stranded DNA
genomes: the genome is double-stranded
DNA, so mRNA is synthesized in the normal
fashion using negative-strand DNA as a
template. Examples: Adenovirus, Hepatitis B
virus
14. Class II viruses, single-stranded DNA
genones: the genome is single-stranded DNA.
Form a double stranded DNA intermediate
during replication and this intermediate used
for transcription. Examples: parvovirus, maize
streak virus.
Class III viruses, double-stranded RNA
genomes: genome is double-stranded RNA,
one strand of which is therefore equivalent to
mRNA.Examples: reovirus, rotavirus
15. Class IV viruses, positive-strand RNA
genomes: genome is single-stranded RNA that
can serve as mRNA directly, so these are
positive-strand viruses. Examples: poliovirus,
Class V viruses, negative-strand RNA
genomes: the genome is single-stranded RNA
that serve as template for synthesis of viral
mRNA. Since genome is complementary to
mRNAs, these are negative-strand viruses.
Therefore, complementary positive strand is
synthesized by RNA polymerase and used as
mRNA. Examples: rabies virus,mumps virus
16. Class VI viruses, retroviruses:the genome is
positive-strand RNA.This RNA virus require
reverse transcriptase to copy the information
found in RNA to DNA but its expression and
replication require synthesis of a double-
stranded DNA molecule Example: Human
Immunodeficiency Virus (HIV).
Class VII viruses: double-stranded DNA
with RNA intermediate:
Double-stranded DNA genome that replicates
with RNA intermediate. Required reverse
transcriptase.
17.
18. Viral diseases
1) AIDS
Human immunodeficiency virus infection /
acquired immunodeficiency syndrome
(HIV/AIDS) is a disease of human immune
system caused by infection with HIV.
During the initial infection, a person may
experience a brief period of influenza-like
illness. This is typically followed by a
prolonged period without symptoms.
19. As illness progresses, it interferes more and
more with the immune system, making the
person much more likely to get infections,
including opportunistic infections
(e.g. Pneumocystis pneumonia, central nervous
system lymphoma) and
tumors.
20. Modes of HIV/AIDS transmission
Through blood products
Intravenous drug abuse
Sharing needles
Unsterilized blades
Through sexual contact
From mother to baby
22. Natural course of HIV/AIDS
Stage 1 – Primary
Short,occurs 1-6 weeks after infection
Mild symptoms(flu like illness)
Infected person can infect other people
Stage 2 - Asymptomatic
Lasts for an average of ten years
This stage is free from symptoms
There may be swollen glands
The level of HIV in blood drops to low levels
23. Stage 3 – Symptomatic
The immune system deteriorates
Opportunistic infections and cancers start to
appear.
Stage 4 - HIV AIDS
The immune system weakens too much as
CD4 cells decrease in number
25. 2)Hepatitis
Is a medical condition defined by
inflammation of liver and characterized by
presence of inflammatory cells in the tissue of
organ,caused by viruses i.e. Hepatitis
A,B,C,D,E.
Hepatitis A
Pathogenesis
HAV invade into human body by fecal-oral
route, and replicates in the liver. After 10–12
days, virus is present in blood and is excreted
via the biliary system into the feces.
26.
27. Symptoms
Influenza like symptoms
(anorexia,nausea,vomitting,fatigue)
Headcahe and low grade fever
Dark colored urine,Abdominal pain
Treatment
No specific medicine
Take rest, increase fluid intake ,
Vaccine is available(Haverix,Vaqta)
28. Hepatitis B
Pathogenesis
It is transmitted pareterally,perinatally and
sexualy. Virus enters hepatocytes via blood.
Immune response (cytotoxic T cell) to viral
antigens expressed on hepatocyte cell surface
responsible for clinical syndrome
Symptoms
same as Hepatitis A
29. Treatment
Interferon (3 injections per week)or PEG
interferon alpha-2a( once in a week) for 6
months
OR Ribavirin+ Lamivudine or Adevofir
Vaccine is available(Engirex)
30. Hepatitis C
Symptoms
Influenza like symptoms
Pruritis
Severe joint pain
Ascites
Abdominal pain
Treatment
Interferon (3 injections per week)or PEG interferon
alpha-2a( once in a week) for 6 months
If it is not effective then PEG interferon+Ribavirine
OR IFN+ Silymarin
31. 3)Dengue fever
Also know as breakbone fever, is an acute
communicable disease caused by Dengue
viruses (categorize into types 1,2,3,4)
transmitted by mosquitoe Aedes aegypti ,Aedes
albopictus.
32. Pathogenesis
Once virus is in body, immune system
produces antibodies against it that adhere to
structural proteins and inactivate virus, which
inhibits it from infecting macrophages. This
stage is when a primary infection occurs, also
known as febrile illness, or dengue fever
Upon exposure to a different serotype of
dengue, immune system attacks in same way
it did to first serotype.
33. However, because surface proteins of each
serotype differ slightly, antibody adherence
does not inactivate virus
It invades macrophages and induces release of
cytokines which causes a more severe
secondary infection, such as DHF.
In addition, dengue viruses have M
proteins that aid in apoptosis of their target cell
34. Symptoms
Dengue starts with chills, headache, pain upon
moving the eyes, and low backache
Painful aching in legs and joints
The temperature rises quickly as high as 104 F
(40 C), with relatively low heart rate and low
blood pressure
35. Dengue hemorrhagic fever is a more severe
form of viral illness.
Symptoms include headache, fever, rash, and
evidence of hemorrhage in the body.
Petechiae (small red or purple splotches or
blisters under the skin), bleeding in the nose or
gums, black stools are all possible signs of
hemorrhage.
36. Management of DF Fever
Is mainly symptomatic and supportive.
1)Bed rest
2)Antipyretics and Analgesics for control of
fever and pain
3)Oral fluid and electrolyte therepy for
excessive sweating and vomiting.
37. Management of DHF Fever
1)Antipyretics and Analgesics for control of
fever and pain
2) Oral fluid and electrolyte therapy for
excessive sweating and vomiting
3) IV fluid therapy to control plasma loss and
impending shock like Iv Colloid, Crystalloid.
38. 4)Chicken pox
An infectious disease causing a mild fever and
a rash of itchy inflamed pimples which turn to
blisters and then loose scabs. It is caused by
the Varicella zoster virus(VZV) and mainly
affects children.
39. Pathogenesis
VZV enters through respiratory tract
It replicate at the site of entry in nasopharynx
and in regional lymph nodes.
A primary viremia occurs 4 to 6 days after
infection and disseminates virus to other
organs,e.g. liver, spleen, and sensory ganglia.
Further replication, causes secondary viremia,
with viral infection of skin.
40. Symptoms
Rash that turns into itchy, fluid-filled blisters
that eventually turn into scabs.
High fever
Tiredness
Loss of appetite
Headache
41.
42. Treatment
Acyclovir can shorten or combat varicella
infection if it is started within 24 hours of rash
development.
43. Prevention
CDC recommends two doses of chickenpox
vaccine.
Children should receive two doses—the first
dose at 12 -15 months and a second dose at 4-
6 years of age.
Varicella-zoster immunoglobulin (VZIG)
contains antibodies to the chickenpox virus.
44. 5)Rabies
It is acute viral disease of CNS. The
causative agent of rabies is rabies virus (RV), a
negative-stranded RNA virus of the
rhabdovirus family
45. Mode of Transmission
Animal bite,Licks
Persin to person
Pathogenesis
Is an acute infection of CNS .Following
inoculation, virus replicates in striated or
connective tissue at site of inoculation and
enters peripheral nerves through
neuromuscular junction.
It then spreads to CNS.
49. Pre exposure prophylaxis
1)Active immunization (Vaccine)
On days: 0, 7, 21,28
2)Booster doses
Post exposure prophylaxis
1)Wound cleaning
2)Passive immunization
HRIG 20IU/Kg IM on day 0
3)Active immunization
On day :0,3,7,14,28
50. 6)Poliomyelitis
Polio gray matter
Myelitis inflammation of the spinal cord
This disease result in destruction of motor
neurons caused by polio virus.It attacks the
nerve cells of the brain & spinal cord
51. Pathogenesis
Poliovirus enters body through mouth,
infecting pharynx and intestinal mucosa.
The virus then hijacks the host cell's own
machinery, and begins to replicate.
Divides within GIT ,from where it spreads to
tonsils,intestinal lymphoid tissue where it
multiplies.
The virus is subsequently absorbed into the
bloodstream.(viremia)
52. It can survive and multiply within blood and
lymphatics
This sustained replication causes a major
viremia
Rarely, this may progress and virus may
invade central nervous system, provoking a
local inflammatory response.
In most cases, this causes a self-limiting
inflammation of meninges,which is known as
nonparalytic aseptic meningitis
53. Symptoms
Many include fever, pharyngitis, headache,
anorexia, nausea, and vomiting. Ilness may
progress to aseptic meningitis and
menigoencephalitis .
These patients develop a higher fever and
sever headache with stiffness of neck and
back.
Paralysis of respiratory muscles can occur or
from cardiac arrest if the neurons in the
medulla oblongata are destroyed.
54. Treatment
Bed rest with close monitoring of respiratory and
cardiovascular functioning is essential during the
acute stage of poliomyelitis along with fever
control and muscle relexants.Mechanical
ventilation, respiratory therapy may be needed
depending on severity of patients.
Vaccine
There are two types of vaccine that protect against
polio: inactivated polio vaccine (IPV) and oral
polio vaccine (OPV). IPV is given as an injection
in the leg or arm.
55. 7)Measles (Rubeola)
It is an acute viral infection characterized by a
final stage with a maculopapular rash erupting
successively over the neck and face, trunk,
arms, and legs, and accompanied by a high
fever. It is caused by infection with the
Rubeola virus, a paramyxovirus of the genus
Morbillivirus.
56. Pathogenesis and clinical features
Virus infects epithelial cells of nose and
conjunctiva. Virus multiplies in them and then
extends to regional lymph nodes.
Primary viraemia occurs 2 to 3 days after
infection, and virus continues to replicate in
epithelial and reticuloendothelial system tissue
over next few days.
Secondary viraemia occurs on days 5 to 7, and
infection becomes established in skin and other
tissues including respiratory tract on days 7 to
11
57. The prodromal phase, which lasts 2 to 4 days,
occurs at this time with fever, malaise, cough,
coryza, and conjunctivitis.
Koplik's spots(very small grayish-white spots
with bluish-white centers in the mouth, insides
of cheeks, and throat)may develop on buccal
mucosa about 1 to 2 days before rash and may
be apparent for 1 to 2 days after rash onset.
58.
59. The rash then develops at about 14 days after
infection; at this time virus can be found in
blood, skin, respiratory tract, and other organs.
Over next few days, viraemia gradually
decreases as rash gradually resolves along
with other signs and symptoms.
Viraemia and presence of virus in tissue and
organs ceases by days 15 to 17 corresponding
to appearance of antibody
60. Treatment
It is an acute self-limiting disease .However
immunocompromised and undernourished,
patients can be protected by
Administration of human anti-measles gamma
globulin if given within the first 3 days after
exposure.
Alternatively, exposed individual can simply
be vaccinated within 72 hours of exposure.
Treatment for symptoms includes plenty of
fluids and paracetamol for the fever
61. Vaccine
The initial measles immunization, usually as
measles-mumps-rubella ( MMR ) vaccine , is
recommended at 12-15 month of age
MMR vaccine may be given for Measles post
exposure
A second immunization , also as MMR, is
recommended routinely at 4-6 year of age
62. Reference
Warren Levinson(2012).
Review of Medical Microbiology and
Immunology(12th edition)
www.slideshare.net/AliaNajiha1/chapter-2-
classification-of-virus
pathmicro.med.sc.edu/lecture/hiv3.htm
Aidsinfo.nih.gov/education-materials/fact-
sheets/19/73/the-hiv-life-cycle