It Contains Pathogenesis of viral diseases like AIDS, Hepatitis, Influenza and Rabies. It contains detail pathogenesis with various verified sources. You can refer references to visit the sources used.

5. Virus was first discovered
by Dmitri Ivanowsky in 1892.
He recognised an infectious
agent, which caused tobacco
mosaic disease and were
smaller than bacteria. M.W.
Beijerinek in 1898 called the
filter 'Contagium vivum
fluidum' and named it the
'virus'.
DIMITRY IVANOWSKY
M.W BEIJERIENK

7. Viruses which are pathogenic towards plants
Example : Tobacco Mosaic Virus, Cauliflower Mosaic Virus
Viruses which are pathogenic towards plants
Example : Small Pox virus, Influenza virus
Viruses which are pathogenic towards bacteria
Example : T- phages, Lambda phages

8. Pathogenesis
Pathogenesis is the process by which an infection leads to disease
or
The manner of development of a disease
It is four step process :-
1. Entry of virus in host body / infection
2. Viral multiplication in host body
3. Spread of virus to target organs
4. Shedding of virus into the environment

9. AQUIRED IMMUNO DEFFISIENCY SYNDROM
TO
OBTAIN
OR LEARN
OR
DEVELOP
FAILURE OF ONCE IMMUNE
SYSTEM TO PROTECT AGAINTS
FOREIGN INVASION
A SET OF
SYMPTOMS
WHICH OCCUR
TOGETHER

10.  This disease is generally caused by HIV (
human immunodeficiency ) virus specifically
Retrovirus HIV-1 in humans.
 HIV belongs to lentivirus family which is a
subgroup of Retrovirus
 The other causative can be HLTV-1 (human
T-cell lymphotropic virus I ), HIV-2 etc.
 Simian immunodeficiency virus ( SIV ) ,
Feline immunodeficiency virus ( FIV ) ,
Bovine immunodeficiency virus ( BIV ) etc
are other immunodeficiency viruses which
infects various animals.
1. Unprotected sexual intercourse & homosexuality .
2. Infected mother to child.
3. Receipt of infected blood or blood products.
4. Sharing of hypodermic needles between intravenous drug
users.
HIV/AIDS cannot be spread through:
•Saliva
•Sweat
•Tears
•Casual contact, such as sharing food utensils, towels, and
bedding
•Swimming pools
•Telephones
•Toilet seats
•Biting insects (such as mosquitoes) etc.
Twenty years ago, on June 5, 1981, MMWR published a report
of five cases of Pneumocystis carinii pneumonia (PCP) among
previously healthy young men in Los Angeles.
By the end of the year 1981, 121 people were known to
have died from AIDS. In 1983, the virus that causes AIDS,
that is HIV (Human immunodeficiency virus)was
discovered
DISCOVERY

11. STRUCTURE OF HIV VIRION
 ENVELOPE :-
• The HIV virion is enveloped and contains 72 external spikes
which are made up of glycoproteins specifically gp120 &
gp41.
• These glycoprotein units has function of attachment to the
specific receptors present on the host cell membrane. These
receptors are CD4 & CCR5
• The envelope is bilayer structure made of lipid.
 CORE :-
• The HIV virion core is made up of protein.
• Core of HIV contain four type of nucleocapsid protein. p24
form chief component of inner shell of nucleocapsid.p17
associated with inner surface of lipid bilayer & stabilise
exterior and interior components of virion. p7 proteins
binds directly to genomic RNA & together with p9 forms the
core.
 GENETIC MATERIAL :-
• Retrovirus core contains two copies of single stranded HIV
genomic RNA to which performed viral reverse
transcriptase, integrase & protease enzymes are attached.

12. how does HIV cause AIDS?
It is a stepwise process
Step 1 : Attachment of virus to specific receptors
Step 2 : Entry of virus into the host cell
Step 3 : Replication of viral genetic material with
the host genetic material
Step 4 : Cell death and spread of disease &
symptoms

13.  Virus enter into the host body through
genital tract, blood etc.
 HIV virion requires specific site on the
host cell to attach through its gp120 spikes
present on the surface of envelop of
virion.
 The virus’s gp120 envelope protein binds
the CD4 glycoprotein in the plasma
membranes of CD4+ T cells, macrophages,
dendritic cells, and monocytes. Because
dendritic cells are present throughout the
body’s mucosal surfaces and bear the CD4
protein, these are likely the first cells
infected by HIV in sexual transmission.
 HIV enters host cells by endocytosis as
well as membrane fusion.
 When gaining entrance by
endocytosis, the virus uncoat from
within the endocytic compartment as
the viral envelope fuses with the
endosome membrane, releasing the
virion contents into the cytosol.

14.  RNA is copied into a single strand of DNA by the RNA-dependent DNA polymerase
activity of the reverse transcriptase enzyme
 The newly synthesized DNA strand now serves as template to form a double-stranded
DNA copy of the original RNA genome also performed by reverse trancriptase.
 A complex of the double-stranded DNA (provirus) and integrase enzyme moves into the
nucleus. Integrase catalyzes the integration of viral DNA into the cell’s DNA once
integrated the viral genome is known as a provirus.
 The provirus can remain latent, giving no clinical sign of its presence. In this stage
virus produces billions of copies.
 Alternatively the provirus can force the cell to synthesize viral mRNA. Some of the RNA
is translated by host cell ribosomes to produce a long polypeptide that is cleaved into
individual proteins by a viral protease. These proteins complete the assembly of new
virions that bud from the infected host cell.
 Eventually the host cell dies.

15.  Once a person becomes infected with HIV, the course of disease can vary greatly.
 The acute infection stage occurs 2 to 8 weeks after HIV infection.
 About 70% of individuals in this stage experience a brief illness referred to as acute
retroviral syndrome, with symptoms that may include fever, malaria, headache,
macular (small, red, spotty) rash, weight loss, and lymph node enlargement
(lymphadenopathy).
 During this stage, the virus multiplies rapidly and disseminates to lymphoid tissues
throughout the body, until an acquired immune response is generated to reduce virus
multiplication.
 The asymptomatic stage of HIV infection may last from 6 months to 10 years. In this
stage there is decline in immune response is observed.
 During the chronic symptomatic stage, which can last for months to years, virus
multiplication continues and the number of CD4+ T cells begins to significantly
decrease.

17. Blood tests are the most common way to diagnose the human immunodeficiency virus (HIV), the virus that
causes acquired immunodeficiency syndrome (AIDS). These tests look for antibodies to the virus that are
present in the blood of infected individuals.
The primary tests for diagnosing HIV and AIDs include:
• ELISA Test : ELISA, which stands for enzyme-linked immunosorbent assay, is used to detect HIV infection.
If an ELISA test is positive, the Western blot test is usually administered to confirm the diagnosis
• Viral Load Test : This test measures the amount of HIV in your blood. Generally, it's used to monitor
treatment progress or detect early HIV infection. Three technologies measure HIV viral load in the blood —
reverse transcription polymerase chain reaction (RT-PCR), branched DNA (bDNA) and nucleic acid
sequence-based amplification assay (NASBA).

19.  There is no cure for HIV infection. Even when viral loads are undetectable, the virus cannot be
eradicated from long-lived resting memory CD4+ T cells. Thus the goal of treatment is to
reduce viral load to undetectable levels, which eliminates disease burden on the patient and
prevents transmission. Importantly, if a patient stops taking antiviral medications, the reservoir
of quiescent CD4+ T cells will become productive hosts and the viral load will rebound to high
levels
 Prevention and control of HIV are achieved primarily through education. Understanding risk
factors and practicing strategies to reduce risk are essential in the fight against HIV.
 Barrier protection from blood and body fluids greatly limits risk of HIV infection.
 HIV-positive mothers need not transmit the virus to their infant if treated with antiretroviral
therapy prenatally and are then educated about breastmilk transmission
 Individuals at high risk of acquiring HIV should be offered the opportunity to take preexposure
prophylaxis (PrEP), a combination of two antiviral agents that dramatically reduces the
probability of transmission.
 Education to prevent the sharing of intravenous needles and syringes is also very important.
 The public should also understand that blood and blood products are screened to prevent HIV
transmission.

21.  It is commonly caused by virus known as
hepatitis virus which belongs to
picornavirus family.
 Five types of hepatitis have been
identified which are hepatitis A, B, C, D, E.
 Hepatitis A is always an acute, short term
disease, whereas hepatitis B,C & D are
most likely to become ongoing & chronic
and hepatitis E is acute but can be
particularly dangerous in pregnant
women

23.  It is a highly contagious liver infection caused by hepatitis A
virus (HAV) which belongs to enterovirus.
 HAV has RNA as genetic material.
 It can cause acute hepatitis with jaundice. Also cause acute
liver failure. It does not cause long term infection.
 Incubation period is 3-5 weeks with an average of 28 days.
 It is transmitted through the faecal-oral route.
 It is more prevalent in underdeveloped courtiers
 The source of infection is crowded conditions, poor personal
hygiene, poor sanitation, contaminated food, water etc.

24. SYMPTOMS
Fatigue
Fever
Abdominal pain
Nausea
Jaundice
Weight loss
Itching
Sharp pain in right upper
quadrant of abdomen
 No antiviral therapy is available. Active
immunization with a vaccine containing
inactivated HAV is available
 The detection of IgM antibody is the most
important test.

25.  Hepatitis B virus can cause acute & chronic
infection.
 Hepatitis B virus (HBV) is a member of
the hepadnavirus family.
 Hep B infection can last up to 6 months and infected
person are able to pass these virus this time.
 Source of infection are contaminated needles,
syringes, blood products.
 Occurrence is for all ages, but mostly affects young
adults worldwide
 Most common among all hepatitis.

26. SYMPTOMS
Abdominal pain
Dark urine
Fever
Joint pain
Loss of appetite
Nausea
Fatigue
jaundice
The two most important serologic tests for the diagnosis of
early hepatitis B are the tests for HBsAg and for IgM antibody
to the core antigen. Both appear in the serum early in the
disease. HBsAg appears during the incubation period and is
detectable in most patients during the prodrome and acute
disease
No antiviral therapy is typically used in acute hepatitis B. For
chronic hepatitis B, entecavir (Baraclude) or tenofovir (Viread)
are the drugs of choice. They are nucleoside analogues that
inhibit the reverse transcriptase of HBV

27. Hepatitis c is an RNA virus whose incubation
period is about 14 – 180 days.
 It is member of Flaviviridae.
In most cases it is transmitted through blood
or blood products.
It can result in both acute and chronic illness
There is no vaccination for HCV
Chronic HCV infection results in liver cirrhosis

28. It is also known as Delta hepatitis
Hepatitis D virus has defective single
stranded RNA virus that can not survive
on its own. It requires hepatitis B to
replicate
Sources of infection are same as HBV
HDV infection is only possible if a person
is already infected with hepatitis B

29. Hepatitis E virus (HEV) is an RNA virus
with incubation period of 15-16 days
It is more common in adults and sever in
pregnant women.
It is most common in developing
countries.
Its structure resembles HAV.

30.  The virus particle consists of an outer
lipid envelope and an icosahedral
nucleocapsid core composed of core
protein
 These virions are 30–42 nm in diameter.
The nucleocapsid encloses the viral
genetic material which can be DNA or
RNA.
 The outer envelope contains embedded
proteins that are involved in viral binding
of, and entry into, susceptible cells

32. STEP 1 : The virus enters the blood stream and infects hepatocytes.
STEP 2 : The virus gains entry into the hepatocytes by binding on the host cell
surface by specific receptors and being endocytosed
STEP 3 : The virus relies its genetic material ( which can be either DNA or RNA )
into the cytoplasm of the host cell.
STEP 4 : In the case of Hepatitis B genetic material is DNA which is partially
double stranded.
STEP 5 : For replication process it goes into the nucleus where it become fully
double stranded by viral polymerase and transformed into covalently closed
circular DNA ( cccDNA ). Thus cccDNA serves as a template for transcription of
four viral RNAs by host RNA polymerase.
STEP 6 : The largest RNA is used to make the new copies of the genome and to
make the capsid core protein and the viral DNA polymerase.
STEP 7 : The long RNA is then transported back to the cytoplasm where the virion
P protein synthesizes DNA via its reverse transcriptase activity .
STEP 8 : By cell lysis is released out and spread into to the body form the blood
stream releasing some cytokines producing symptoms of disease. At the end liver
get damage.

35.  The influenza virus infects the
upper respiratory tract and major
central airways in humans,
horses, birds, pigs, and even
Seals.
 Between 1918 and 1919, the
largest influenza pandemic
(worldwide epidemic) in recent
history occurred, killing between
20 million and 50 million people.
 There are four types of influenza
viruses :- TYPE A, TYPE B, TYPE C
& TYPE D
 Among them all TYPE A & B are
the most common types
Chills
Fever
Sore
Throat
Muscle pain
Severe headache
Coughing
Fatigue

36. SIZE : 80-200nm in diameter
ENVELOP : A lipid bilayer having some protein
constituents.
Two viral Glycoproteins are imbedded in this envelop
which are hemagglutinin (HA) & neuraminidase (NA).
HA is responsible for the attachment of the virus to host
cells. NA facilitates viral budding from the infected host
cell.
NUCLEO CAPSID :- This structure is made of protein and
encloses viral genetic material.
GENETIC MATERIAL : It consists of eight different strands
od ssRNA associated with protein and RNA polymerase.
Each RNA strand encodes one or more different influenza
protein.

37. Influenza can be difficult to diagnose, because its most visible symptoms (fever, cough, aches) are similar
to many other common illnesses. Healthcare providers have several different ways to determine if a
patient has the flu. Rapid influenza diagnostic tests can detect influenza in under 30 minutes, using
swabs or samples of secretions taken from a patient’s nose or throat. However, these tests can yield false
positive or false negative results, and they may not be able to indicate which specific strain of flu the
patient has.
Common testing methods include viral culture, rapid antigen testing and rapid molecular assays using
reverse transcription polymerase chain reaction (PCR)
For patients that are not in a high risk group, treatment focuses on relieving symptoms of
influenza such as fever. Patients that are known to be in a group at high risk for developing
severe or complicated illness should seek medical attention and should be treated with antiviral
drug as soon as possible.

39. 1. Influenza virus is transmitted from person to person primarily in droplets released by sneezing and coughing.
2. Following respiratory transmission, the virus attaches to the sialic acid receptors on the epithelial cells by HA
present on the viral envelop and penetrates respiratory epithelial cells in the trachea and bronchi.
3. Virus get endocytosed & and fusion and uncoating of viral body takes place.
4. Viral RNA get associated with host cell RNA & protein synthesis can takes place
5. Viral replication occurs, which results in the destruction of the host cell. Regeneration of epithelium takes
about 3 to 4 weeks.
6. Neuraminidase of the viral envelope may act on the N-acetyl neuraminic acid residues in mucus to produce
liquefaction.
7. In concert with mucociliary transport, this liquefied mucus may help spread the virus through the respiratory
tract.
8. Infection of mucosal cells results in cellular destruction and desquamation of the superficial mucosa.
9. The resulting edema and mononuclear cell infiltration of the involved areas are accompanied by symptoms
including nonproductive cough, sore throat, and nasal discharge.
10. Viremia, or presence of virus in the blood, has rarely been documented.
11. Virus is shed in respiratory secretions for 5 to 10 days, with a peak of 1 to 3 days following illness onset.

41.  The causative agent of rabies is rabies virus (RV) which is
negative stranded RNA virus of the rhabdovirus family.
 In most cases the disease is transmitted via the bite of rabid
animals which shed infectious virus with their saliva.
 The virus enters the body through transdermal inoculation or
direct contact of infectious material to mucous membranes or
skin lesions.
 Five general stages are recognized in humans : incubation,
prodrome, acute neurologic period, coma and death.
 The incubation period is exceptionally variable ranging from
fewer than 10 days to longer than 2 years but is usually 1-3
months.

42.  Shape : Rabies virus is rod shaped. Bullet shaped one
end conical and other planner
 Envelope : Virus envelope contains glycosylated G-
protein spikes embedded in a lipid membrane derived
from the host cell. This envelope doesn’t cover the
planar end
 Matrix protein : The membrane or matrix protein layer
lies beneath the envelope. Virus nucleoprotein (N)
which tightly binds the viral RNA to form the
nucleocapsid core lies inside to matrix protein
 Viral genome :The core of the virion consists of helical
RNP (group-specific antigen). The genome is
unsegmented, linear, ss (-) sense RNA and the virion
contains an RNA-dependent RNA polymerase.

43. Symptoms include fever, headache, excess
salivation, muscle spasms, paralysis and
mental confusion
◗ Specimens Saliva, serum,
cerebrospinal fluid (CSF), blood, urine,
and skin and brain biopsy are the
frequently used specimens for
diagnosis of rabies.
◗ Microscopy Demonstration of Negri
bodies by microscopy is the
characteristic histopathological feature
of rabies. Impression smears of the
human brain tissue collected at post-
mortem are stained by Seller’s
technique for demonstration of Negri
bodies. The stain contains methylene
blue alcohol as fixative and basic
fuchsin as staining reagent.
No specific anti rabies agent is available.
Although until recently rabies was considered
to be invariably fatal, it has now been
demonstrated that complete recovery can
occur from established rabies with intensive
supportive care and management of
complications

45. • The virus may enter the peripheral nervous system directly at the site of bite
In some cases, however, it may replicate in muscle tissue after entering the host, remaining at
or near the site of introduction for most of the incubation period
• The virus infects the sensory neurons and moves rapidly by axonal transport centripetally to
the central nervous system (CNS) for replication.
• During its transport within the neurons, it is protected from the host immune system
• The virus travels along the axons at a rate of 12–24 mm in a day to enter the spinal ganglion.
• Its multiplication in the ganglion is indicated by the onset of pain or paresthesia at the site of
the inoculum, which are the first clinical symptom and a hallmark finding
• From here, the virus spreads quickly, at a rate of 200–400 mm/day, into the CNS, and the
spread is marked by rapidly progressive encephalitis.
• Thereafter, the virus spreads to the periphery and salivary glands
• During the course of infection, encephalitis develops, associated with the death of neurons
and demyelination.

46. REFRENCES
Prescott’s Microbiology
Kuby Immunology
Unified Botany B.Sc 1st year Shivlal Agrawal & Company
Microbiology and immunology by Subhash Chandra Parija
Review of Medical Microbiology and Immunology by Warren E Levinson
https://www.ncbi.nlm.nih.gov/books/NBK8149/#:~:text=Pathogenesis%20is%2
0the%20process%20by,of%20virus%20into%20the%20environment.
https://stanfordhealthcare.org/medical-conditions/sexual-and-reproductive-
health/hiv-aids/causes.html

47. https://www.slideshare.net/NikhilVaishnav3/hepatitis-128140979
https://www.slideshare.net/BasheerOudah/hepatitis-b-69695516
https://en.wikipedia.org/wiki/Hepatitis_B
https://www.who.int/news-room/fact-sheets/detail/influenza-
(seasonal)

48. https://www.ncbi.nlm.nih.gov/books/NBK8618/#:~:text=Pathogenesis,n
ervous%20system%20invasion%20and%20replication.
https://microbeonline.com/virology-note-rabies-virus-structure-
pathogenesis-and-clinical-findings/
https://www.niaid.nih.gov/diseases-conditions/influenza-
diagnosis#:~:text=Rapid%20influenza%20diagnostic%20tests%20can,of
%20flu%20the%20patient%20has.
https://www.ucsfhealth.org/conditions/aids/diagnosis#:~:text=The%20
primary%20tests%20for%20diagnosing,administered%20to%20confirm
%20the%20diagnosis.