A Chronic Lyme Disease Co-infection And Cancer Causing Agent, Cytomegalovirus: Weak Immune System & Chronic Fatigue

Statistics indicate that approximately 80 percent of adults in the United States are infected with cytomegalovirus (CMV) – a virus that affects a majority of individuals, irrespective of locale. CMV is a member of the herpes family and shares the common ability to remaining alive, yet dormant, in the human body for the life of its human host. Rarely does CMV become active unless the immune system is compromised and is rendered incapable of inhibiting the virus. Trauma or weakening the immune system through complex conditions such as Lyme disease could instigate an awakening of CMV.

==> How is CMV spread the Contagious co- viral infection of Chronic Lyme disease

CMV manifests itself by direct individual contact. The virus is present in various bodily fluids, including urine, blood, saliva, semen, cervical secretions, and breast milk. It can also be transferred from a pregnant woman to her fetus. The best way to prevent contraction of CMV is through conscientious hygiene practices, such as regular hand washing.

==> Pathogenesis of CMV Replication Bring About Chronic Fatigue Syndrome

The CMV genome is composed of lineal, double-stranded DNA and surrounded by a protein lining called “matrix” which contains phosphoproteins that are highly capable of deregulating the host’s cellular cycle. This lining is surrounded by glycoproteins deemed vital for various aspects of the virus’s infectivity, including: entrance to the host cell, cell-to-cell dissemination, and maturation.

The fusion between the virus with the cell is mediated by the viral glycoprotein. The fusion is followed by the entrance of the nucleocapsid and protein lining of the host cell cytoplasm. The nuclei are quickly translocated, providing an infection marker which assures detection in serum within one hour. The main reservoirs of CMV are the fibroblasts, myeloid cells, and endothelial cells. The infection of endothelial cells and macrophages plays a critical role in latency, and seems to be essential for maintaining CMV in the host.

Replication typically begins within 12-24 hours after cell infection, and the cytopathic effect in the viral culture can be seen after 7-14 days. As with other herpes viruses, CMV invades the host cell, inhibits protein synthesis, and liberates viral DNA to the nuclei where replication can ensue.. An agenda that CMV shares with other herpes viruses is its ability to thwart the host immune response by inhibiting RNA formation – thereby blocking the presentation of antigenic peptides on the cells’ surface, and preventing apoptosis. These mechanisms can prompt a latent infection to reactivate – oftentimes in transplant recipients.

==> Weakened Immune Systems is Part of this Disease Complex of this and other co-viral activations found Chronic Lyme disease

CMV is relatively harmless for most of the population. However, for those individuals who already bear the risk of a weakened immune system, the virus can stimulate severe disease. Those who are at the greatest peril for active CMV infections and its resultant complications are as follows:

==> cancer patients in active receipt of chemotherapy

==> organ transplant recipients

==> persons stricken with HIV infections

==> babies born to women exposed to CMV while pregnant

==> individuals suffering with Chronic Lyme disease

==> Symptoms Related to CMV making Chronic Fatigue and Chronic Lyme disease Difficult for Patients.

The unpleasant signs and symptoms of a CMV infection in children and adults include: prolonged high fever, chills, severe fatigue, an overall ill feeling, swollen lymph glands, headache, and an enlarged spleen. People with weakened immune systems are at risk for more serious complications including pneumonia, liver infection, anemia, and in some cases, death. In patients with HIV, CMV can infect the retinas and promote blindness. In newborns, CMV infection can prompt mental and developmental problems and/or affect vision and hearing. Most infected newborns do not demonstrate signs of the infection at birth, but such symptoms may appear over the next several years.

At Envita, we provide therapies plucked from around the world that can help shorten healing time and boost the immune systems for those with Cytomegalovirus. The Company’s state-of-the-art diagnostic tools can quickly identify and correct misdiagnoses for those with CMV, affording them the opportunity to obtain effective treatment for their condition while experiencing much-needed relief.

==> Ovarian Carcinoma – CMV Virus What causes Cancer?

A study was conducted with women suffering with epithelial ovarian carcinomas who were infected with human papillomavirus (HPV), Chlamydia trachomatis, and cytomegalovirus (CMV). A total of 39 tissue samples were analyzed with consensus and type-specific primers for HPV, primers specific for Chlamydia’s cryptic plasmid, as well as primers for glycoprotein B of CMV.

Results showed 40, 80, and 50 percent positivity for HPV, Chlamydia, and CMV infections, respectively, in cancerous ovarian tissues. The HPV type detected was HPV-6, with its genome integrated to the host genome in the case of both invasive and borderline tumor. Infectious genetic information was recognized even among the healthy controls.

The patients with Chlamydia and CMV infections were found to have significantly higher risk of developing ovarian tumors. Findings validate the premise that chronic infections and inflammation are involved in the pathogenesis of epithelial ovarian cancer. This study is theprototype for detecting the bacterial and viral causatives of ovarian carcinoma development – a concept supported by Envita for years. In simple terms, infections and chronic inflammation can in fact cause cancer. Envita Medical Centers desires to treat both cancer and its causative agents such as infection.

The essence of treating CMV is to establish a strong immune system and desseminate other infection agents responsible for the patient’s compromised immune state. For more information on the world’s foremost treatments for cancer and infections such as CMV, contact Envita Medical Centers now.

==> References:

Stern, J.L., Slobedman, B. Human cytomegalovirus latent infection of myeloid cells directs monocyte migration by up-regulating monocyte chemotactic protein-1. J. Immunol. 2008 May 15; 180(10): 6577-85.

Slobedman, B., Cheung, A.K. Microarrays for the study of viral gene expression during human cytomegalovirus latent infection. Methods Mol. Med. 2008; 141: 153-75.

Domenech, E., et al. Cytomegalovirus infection in ulcerative colitis: A prospective, comparative study on prevalence and diagnostic strategy. Inflamm. Bowel Dis. 2008 May 1 (Epub).

Trends Transplant. 2009
Landolfo S, Gariglio M, Gribaudo G, Lembo D. The human cytomegalovirus. Pharmacol Ther. 2003;98:269-97

Rowshani AT, Bemelman FJ, van Leeuwen EM, van Lier RA, ten Berge IJ. Clinical and immunologic aspects of CMV infection in solid organ transplant recipients. Transplantation. 2005;79:381-6.

Jarvis MA, Nelson JA. Human CMV persistence and latency in endothelial cells and macrophages. Curr Opin Microbiol. 2002;5:403-7.

==> Viral and bacterial aetiologies of epithelial Ovarian Carcinoma

Department of Biochemistry, School of Life Sciences, Bharathidasan University, Tiruchirappalli, Tamilnadu, India.

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