Introduction

A.History
• A.History of the Disease. Rubella was at first considered to be a variant of the measles or
scarlet fever and was called 3rd disease. The name Rubella comes from the Latin word
meaning “little red.” In 1814, it was first discovered to be a separate disease from the
measles in German medical literature thus receiving its nickname the “German measles.” In
1912, measles became a nationally notifiable disease in the United States, requiring U.S.
healthcare providers and laboratories to report all diagnosed cases. In the first decade of
reporting, an average of 6,000 measles-related deaths were reported each year. In 1914,
Hess postulated a viral etiology, and in 1938, Hiro and Tosaka confirmed his etiology by
passing the disease to children with nasal washings from an infected person with an acute
case. In 1941, Norman Gregg reported congenital cataracts in 78 infants whose mothers
had maternal rubella in early pregnancy. These were the first cases reported of congenital
rubella syndrome (CRS) .In 1962, rubella was first isolated by Parkman and Weller who then
went on to find the general characteristics of the virus. In the decade before 1963 when a
vaccine became available, nearly all children got measles by the time they were 15 years of
age. It is estimated 3 to 4 million people in the United States were infected each year. Also
each year an estimated 400 to 500 people died, 48,000 were hospitalized, and 4,000
suffered encephalitis (swelling of the brain) from measles.
 B. Introduction of this virus.
• Rubella is caused by RNA virus and has a peak age of 15 years the
incubation period is 14-21 days. Rubella Virus is only known to infect
humans and is responsible for the common childhood disease known as
German Measles or Three Day Measles because of its short duration. The
disease presents primarily as a skin rash, fever, lymphadenopathy with
other mild symptoms in adults who contract the disease. Rubella can
also cause arthritic symptoms, most commonly in women Rubella Virus
can be prevented with the MMR (Measles, Mumps, Rubella) Vaccine
which makes the virus uncommon in countries where vaccines are
available. Rubella Virus can cause serious harm to unborn fetuses of
mothers who contract Rubella Virus within the first trimester. The virus
causes CRS (Congenital Rubella Syndrome) causing birth defects. CRS can
cause a variety of birth defects and can lead to miscarriage or stillbirth.
 C. The distribution of this disease.
• Worldwide. Now rubella is rare in locations
where vaccination is standard practice.
Countries with standard rubella vaccination
are shown in blue color.
 D.Epidemic.
• D.Epidemic. Epidemics occurred roughly every
6-9 years but immunization programs have
greatly reduced the number of cases in
developed countries and the majority of
people who got measles were unvaccinated.
 Classification of the virus
• Togaviridae family
• Rubivirus.(Rubella is the sole member of the
Rubivirus genus
• Circular or oval in shape.
• Size 40- to 80-nm in dimeter.
• Enveloped icosahedral virus.
• Rubella virus is an RNA virus,positive-
sense,singlestranded RNA (+ssRNA ).
 Proteins
• The genomic RNA of rubella virus contains two
long open reading frames (ORF), a 5′- proximal
ORF that codes for the nonstructural proteins
and a 3′-proximal ORF that encodes the
structural protein
 Transmission of Rubella virus
• German Measles is highly contagious and it
lives in the mucus in the nose and throat of
infected people. It can be spread by
respiratory droplets and by direct contact with
secretions from nose and throat of an infected
person when they sneeze, cough or talk,
droplets spray into the air and the droplets
remain active and contagious on infected
surfaces for up to two hours
Penetration and Target organ of Rubella virus

• The virus enters through the respiratory and almost certainly

multiplies the cells of the respiratory tract. Then it extends to local
lymph nodes where virus amplification, during the prodomal stage,
gives rise to giant multinucleated lymphoid or reticuloendothelial
cells (i.e., Warthin–Finkeldy cells). These syncytia, identified in the
submucosal areas of tonsils and pharynx, are thought to be a major
source of virus spread to other organs and tissues through the blood
stream. Subsequent additional replication in selected target organs,
such as the spleen and lymph nodes, leads to a secondary viremia
with wide distribution of rubella virus. A secondary viraemia follows
whereby the virus is further spread to involve the skin, the viscera,
kidney and bladder. At this time the virus can be detected in the
blood and respiratory secretions.
 Entrance of Rubella into the body
Rubella virus 10 THE LIFE CYCLE OF
the VIRUS
 1. Transmission
• The first step of the viral life cycle is transmission to a host
cell. Viruses completely rely on the host organism to carry out
the means of transmission. In many situations, some activity
of the host organism directly transfers the virus to another
organism. Certain viruses are transmitted to a new host by a
vector. In complex animals and plants, viruses are transmitted
from cell to cell within the body as well as transferred to a
new host. Successful transmission means that the virus must
make contact with uninfected host cell. For most viruses, this
means that the virus must enter the body and be transferred
to the particular cells that they infect.
 Adsorption
• Following the transmission step is the adsorption step, which
involves the virus's attachment to the host cell's surface.
Attachment typically occurs on particular cells of the host.
Attachment takes place when viruses come across a cell that
has cell membrane receptors that match the viral attachment
proteins. Many types of receptors are found on the outer
surface of the cell membrane. Receptors carry out many
functions for a cell, including the detection of certain
chemicals such as hormones. Viruses cannot seek out a
particular receptor. They are transmitted randomly to host
cells and by chance may reach a cell that matches their
attachment proteins.
 Penetration
• After adsorption, the viral infection progresses to the
third stage, which is called penetration. Viruses without
an envelope stimulate the cell to engulf the virus. These
viruses attach to a specific cell receptor that causes the
cell to take in the virus. Cells engulf viruses by covering
the virus with a bubble of cell membrane. The cell then
moves the bubble into the cell, swallowing up the virus.
Enveloped viruses enter a cell by fusing with the cell
membrane. Upon fusion, the virus either blends with the
cell or is engulfed in a bubble of cell membrane. The virus
is not yet active at this point of infection.
 Uncoating
• Stage four of infection is the uncoating event. At this stage
the envelope and capsid break apart, releasing the viral
genome into the intracellular fluids. Viral replication cannot
take place without this stage. Researchers have discovered
that once the virus is uncoated, it is very difficult to find the
viral genome in the host cell. Thus, scientists call this the
eclipse phase because the virus is apparently hiding in the
cell. At this stage it is possible for the cell to destroy the
virus using enzymes and other molecules designed to ward
off viral attack. Cells attack viruses using proteins and
nucleic acids that digest viral genetic material.
 Synthesis
• The next stage is called synthesis; at this stage the cell is being
directed by the virus to replicate the viral genome and
capsomeres. This stage varies greatly. Each virus has a specific
synthesis stage based on its genome composition and type of
capsid. The viral genome serves as the blueprint for building the
viral components. Overall, many viruses start the synthesis stage
by first producing repressor proteins that control certain host cell
functions. At this point, the cell is now diseased and does not carry
out many of its vital functions. Some cells die prematurely at this
stage and in turn stop viral replication. In humans, infected cells
usually release signaling proteins that initiate an immune response
targeted at controlling viral replication
 Assembly (maturation phase)
• Viral assembly is the sixth stage of infection. It is some-times called
the maturation phase. This is when the viral parts come together
inside the infected cell to form new viruses. Mul-tiple copies of new
genomes are made using the cell's chemistry for making DNA and
RNA from nucleic acid building blocks in the cell. These copies then
bind to viral proteins to combine the genome copies with
capsomeres. The replicated capsomere proteins selfassemble around
the genome or the nucleocapsid. Other proteins are also made by the
host cell and self-assembled into the capsid structure. Many of the
mature viruses contain defects, including incomplete genomes and
abnormal capsids. The number of defective viruses is insignificant
compared to the number of normal viruses that will move along
successfully to the last stage of infection
 Releasing
• The release phase is the final stage of viral infection. Like the synthesis stage, this stage varies
greatly among the different types of viruses. Some viruses are released from the cell by
programming the cell to undergo lysis, which causes the cell to break down and die. The cell can
be induced into lysis by specific viral proteins. In many cases, a cell undergoes lysis as it slowly
dies over the course of the viral infection. Other viruses remain in the cell for long periods of
time without reaching the release phase. In certain cases, these delayed viruses can cause a cell
to replicate rapidly and produce a tumor. It is possible for some tumors to develop into cancer.
Certain enveloped viruses bud from the cell. The virus forms a bud by being pushed against the
inner surface of the cell until it becomes enveloped in a bubble of cell membrane. The bud is
then released, and this produces a viral capsid surrounded by an envelope that is composed of
cell membrane and viral proteins. Enveloped viruses usually bud slowly, which keeps the cell alive
for the natural lifetime of the cell and produces a persistent infection that results in a long illness.
Much of the illness associated with a viral infection is due to a loss of cell function. Viral
replication prevents the cell from carrying out its functions. Some of these cell functions may
affect the rest of the body. Viruses that infect cells of critical body organs can produce severe
effects on the body and can lead to death. The time it takes to feel ill from a viral infection
depends on the replication speed of the virus. A certain number of cells must be infected before
the body is affected by the nonfunctioning cells
Replication cycle of Rubella Virus