Disruption Of Cytoskeleton And Cell Enlargement Biology Essay

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Cytomegalovirus belongs to herpes virus family which is capable of causing throat infection along with many other infections. Since this virus is capable of disruption of cytoskeleton and cell enlargement, so this virus is called cytomegela virus. The virus has the characteristics to remain in the body after infection.inspite of their living these viruses rarely causes disease until immunity against them is suppressed by using drugs, infection or old age. Immunity against this virus is asymptotic in which there is prolonged, unapparent infection (virus resides in T cells).its symptoms are found similar to mononucleosis. It rarely leads to serious disease, otherwise it usually causes mild symtoms.CMV is mainly a problem for certain high-risk groups, such as mothers suffering from diseases caused by CMV (cytomegalovirus) causes danger for her unborn baby. Children or adults whose immune systems have been weakened by disease or drug treatment, such as organ transplant recipients or people infected with HIV [1].


The symptoms of this infection with the age, person, and health of the person.

Childrens are found free of the symptoms of this virus, after they got infected by CMV

But in few cases symptoms such as birth, premature delivery, jaundice and enlarged liver and spleen is found. These infants are also at risk of developing hearing, vision and neurological problems.

Newborns are also susceptible to CMV infection while passing through birth canal of an infected mother, consuming breast milk of the infected mother or through blood transfusion from CMV infected person.

Older kids and teens who become infected may have mono-like symptoms, including fatigue, muscle aches, headache, fever, and enlarged liver and spleen. These symptoms are generally mild and usually last only 2 to 3 weeks.

CMV can cause serious infections in people who have received organ transplants or those whose immune systems are weakened. In someone with AIDS or HIV, CMV infection may involve the lungs, nervous system, gastrointestinal tract, and the eye, sometimes causing blindness.

CMV infection is a very common infection throughout the world as 4 to 5 person get affected in childhood and some in early adulthood.

Transmission is sexual, congenital (at birth), through blood products or transplantation, and person-to-person (e.g., day care centers).

Immunodeficient patients and those receiving immunosuppressive therapy may develop symptoms of pneumonia (such as fever, cough, or dyspnea), or symptoms of other secondary infections, as mentioned above

Transmission is sexual, congenital (at birth), through blood products or transplantation, and person-to-person (e.g., day care centers).

Most adults exhibit mild, nonspecific clinical signs and symptoms, or none at all. Some adults develop mononucleosis with 2 weeks of irregular high fever.

Immunodeficient patients and those receiving immunosuppressive therapy may develop symptoms of pneumonia (such as fever, cough, or dyspnea), or symptoms of other secondary infections, as mentioned above.

Sore throat, swollen lymph nodes (lymph glands), Fever, Headache, Fatigue, Weakness, and Muscle aches, Loss of appetite.

People suffering from human immunodeficiency virus (HIV) or consuming immunosuppressant medicines have severe symptoms on getting infected by CMV.Such as blindness, pneumonia, diarrhea, bleeding ulcers in the esophagus (windpipe) or intestines, Inflammation of the brain (encephalitis), Seizures.[1,2]


Cytomegalovirus Genomics:

There are two general classes of CMV (cytomegalovirus)

Clinical isolates

Laboratory strains

Most notably, the laboratory strain AD169 appears to lack a 15kb region of the 200kb genome that is present in clinical isolates. AD169 is also unique in that it is unable to enter latency and nearly always assumes lytic growth upon infection [4].

Cytomegalovirus belongs to beta herpes virus sub family. It is the virus with narrow host range. The HCMV genome consists of one long and one short domain .Another open reading frames TRS1 and IRS1 are also there which contain both the repeated and non repeated domains. The transcription of these genes are controlled by identical immediate early promoters pTR1and pIRS1,are the proteins which are found in the virion .A cell after getting infected by the cytomegalovirus is found to have the presence of these two proteins .These proteins pTRS1 and pIRS1undergo transcriptional activation. Both proteins were found to act in conjunction with the immediate-early transcriptional regulatory proteins, IE1 and IE2. More recently, pTRS1 and pIRS1 have been shown to block the double-stranded RNA-dependent protein kinase R response pathway, an antiviral pathway that shuts down protein synthesis in infected cells. Finally, we have shown that pTRS1, but not pIRS1, acts late during the virus replication cycle to facilitate the production of virions [4, 5].

Fig. 1: HCMV (human cytomegalovirus) lytic life cycle.

1, Binding of HCMV glycoprotein gB and gHs to cellular receptors activates cellular transcription factors, such as NF-B and Sp1.

2, The virus then enters the cell, releasing viral DNA, virion proteins and virion mRNA transcripts into the cytoplasm, where virion mRNAs are translated. Viral DNA and certain viral proteins are transported to the nucleus.

3, In the nucleus, viral and cellular genes are expressed, with help from the activated transcription factors, and viral DNA is replicated.

4, Viral DNA, viral and cellular proteins, and virion transcripts are packaged into the virion through an as yet undetermined mechanism. During egression of the virion from the cell, the virion envelope is constructed and an infectious viral particle is released.

The CMV is surrounded by glycoprotein (gB, gN, gO, gH, gM, gL) which are necessary for the infection caused by virus, entrance to the host cell and cell maturation.

The fusion of the virus with the cell is mediated by the viral glycoprotein gB. The fusion occurs with the entry of the nucleocapsid and the lining proteins into the host cell. The main reservoirs for CMV are fibroblasts, myeloid cells and endothelial cells. The infection of endothelial cells and macrophages plays an important role in the latency and this is the critical point in the maintenance of CMV in the host. The process of replication starts after 12 to 24 hours after the infection in the cell.CMV generally invades the host cell, inhibits protein synthesis, and liberates viral DNA into nuclei, where the replication starts immediately.CMV is also capable of stopping the immune response of the host by inhibiting RNA formation, blocking the presentation of antigenic peptides of the cell surface and blocking apoptosis [5].