Epstein infection

FIAC also strongly inhibits HCMV and Epstein-Barr vims (EBV) in vitro the two vimses known not to induce a specific viral thymidine kinase for their repHcation. However, HCMV may stimulate cellular kinases that can anabolize FIAC to its 5 -triphosphate, which specifically inhibits the HCMV-encoded DNA polymerase. This selective activity suggests that FIAC should be evaluated against HCMV infections. FIAC-ttiphosphate incorporated into DNA has shown strong in vitro activity against the DNA polymerases of human hepatitis B vims (HBV) and of woodchuck hepatitis vims (WHV) (37). 

Nasimuzzaman M, Kuroda M, Dohno S, Yamamoto T, Iwatsuki K, Matsuzaki S, Mohammad R, Kumita W, Mizuguchi H, Hayakawa T, Nakamura H, Taguchi T, Wakiguchi H, Imai S (2005) Eradication of Epstein-Barr virus episome and associated inhibition of infected tumor cell growth by adenovirus vector-mediated transduction of dominant-negative EBNAl. Mol Ther 11 578-590... 

Richardson JH, Child LA, Lever AM (1993) Packaging of human immunodeficiency virus type 1 RNA requires cis-acting sequences outside the 5 leader region, J Virol 67 3997 005 Roberts MR, Qin L, Zhang D, Smith DH, Tran AC, Dull TJ, Groopman JE, Capon DJ, Bym RA, Finer MH (1994) Targeting of human immunodeficiency virus-infected cells by CD8-I- T lymphocytes armed with universal T-cell receptors. Blood 84 2878-2889 Rooney CM, Smith CA, Ng CY, Loftin S, Li C, Krance RA, Brenner MK, Heslop HE (1995) Use of gene-modified virus-specific T lymphocytes to control Epstein-Barr-virus-related lympho-proliferation. Lancet 345 9-13... 

Sevigny JJ, Albert SM, McDermott MP, Schifitto G, McArthur JC, Sacktor N, Conant K, Seines OA, Stern Y, McClernon DR, Palumbo D, Kieburtz K, Riggs G, Cohen B, Marder K, Epstein LG (2007) An evaluation of neurocognitive status and markers of immune activation as predictors of time to death in advanced HIV infection. Arch Neurol 64(1) 97-102... 

In advanced AIDS, MM is usually associated with opportunistic infections such as CMV (Said et al. 1991 RouUet et al. 1994 Kolson and Gonzalez-Scarano 2001) or is secondary to lymphoma (Fuller et al. 1993). Despite a role for other herpes viruses in AIDS-associated myelitis, no substantive evidence has been published in support of a role for other vimses in the development of HIV-associated MM, including herpes simplex 1 or 2, varicella zoster, or Epstein Barr vims (Kolson and Gonzalez-Scarano 2001). MM can occur secondary to hepatitis B and C viruses, which are common co-infections of HIV-infected patients, particularly when there is an associated cryoglobulinemia (Taillan et al. 1993 Caniatti et al. 1996). Rarely... 

Saito Y, Sharer LR, Epstein LG, Michaels J, Mintz M, Louder M, Golding K, Cvetkovich TA, Blumberg BM (1994) Overexpression of nef as a marker for restricted HIV-1 infection of astrocytes in postmortem pediatric central nervous tissues. Neurology 44 474-481 Sargeant TJ, Day DJ, Mrkusich EM, Eoo DE, Miller JH (2007) Mu opioid receptors are expressed on radial glia but not migrating neuroblasts in the late embryonic mouse brain. Brain Res 1175 28-38... 

Epstein-Barr virus (EBV) Enveloped, icosahedral particles 150nm in diameter Infections occur by salivary exchange. In young children they are commonly asymptomatic but the virus persists in a latent form in lymphocytes. Infection delayed until adolescence often results in glandularfever. In tropical Africa, a severe EBV infection early in life predisposes the child to malignant facial tumours (Burkitt s lymphoma)... 

Acyclovir [9-(2-hydroxyethoxymethyl)guanine] (ACV) is clinically useful in the treatment of infections caused by several members of the herpes virus (e.g., herpes simplex, varicella zoster and Epstein-Barr virus [2,38,39]). An enzyme coded for by the virus phosphorylates ACV to a monophosphate intermediate. This species in turn undergoes further phosphorylation to a triphosphate with the aid of normal cell enzymes. Then, ACV triphosphate inhibits the herpes virus DNA... 

Checkley W, Epstein LD, Gilman RH, Black RE, Cabrera L, Sterling CR Effects of Cryptosporidium parvum infection in Peruvian children Growth faltering and subsequent catchup growth. Am J Epidemiol 1998,148 497-506. 

Acute inflammatoiy demyelinating polyneuropathy is a common cause of reversible paralysis. Acute inflammatory demyelinating polyneuropathy (AIDP), the classic form of the Guillain-Barre syndrome, often begins a week or two after recovery from cytomegalovirus, Epstein-Barr virus or Mycoplasma infection. Patients present with rapidly advancing symmetrical weakness, loss of deep tendon reflexes, often with distal numbness, and limb or back pain. Cerebrospinal fluid (CSF) protein concentration is elevated, but in most cases there is little or no increase in number of inflammatory cells in the CSF. This albumino-cytologic dissociation contrasts with the elevation of both... 

Li+ has significant inhibitory effects upon DNA viruses, in particular HSV which has been studied in depth. It was originally shown that Li+ inhibits viral replication in a dose-dependent, reversible manner in HSV-infected baby hamster kidney cells [240], and this has been found to be due to a Li+-induced decrease in the synthesis of viral DNA [241]. It is now well established that Li+ inhibits DNA synthesis in HSV types 1 and 2 and in several other DNA viruses, including measles, vaccinia, adenovirus, poxvirus, pseudorabies virus, Epstein-Barr virus, and the bovine, equine, and canine HV s [241]. Interestingly, Li+ has no effect on the replication of RNA viruses, such as influenza or encephalomyo-carditis virus. 

Malignant Reed-Sternberg cells overexpress nuclear factor-K B, which is associated with cell proliferation and anti-apoptotic signals. Infections with viral and bacterial pathogens upregulate nuclear factor-K B. Epstein-Barr virus is found in many, but not all, HL tumors. 

Esterling, B.A. et al., Psychosocial modulation of antibody to Epstein-Barr viral capsid antigen and human herpesvirus type-6 in HIV-1-infected and at-risk gay men, Psychosomat. Med., 54, 354, 1992. 

Hairy Leukoplakia. This is an abnormal condition of the mouth in which white plaques appear on the surfaces of the tongue. These plaques are not due to the overgrowth of a fungus or bacterium. They are due to the abnormal growth of the papillae cells of the tongue. These plaques cannot be scraped off they resemble cancer cells and appear as a result of infection with Epstein-Barr virus, which is a member of the herpes virus family. 

Cytomegalovirus (CMV) is a member of the herpes virus family, as are the varicella zoster and Epstein-Barr viruses described earlier. CMV is a common virus, and many people are infected early in the childhood. Children tend to get an asymptomatic infection, while infected young adults may develop a mono-nucleosis-like illness. Infection of a fetus is very serious and can lead to permanent brain damage or death of the fetus. In AIDS patients, CMV infection can recur and tend to infect the retinas of eyes, leading to blindness. The virus also infects the adrenal gland, leading to hormonal imbalance. CMV pneumonia in patients who have PCP at the same time is usually fatal. 

Leight ER, and Sugden B (2000) EBNA-1 a protein pivotal to latent infection by Epstein-Barr virus. Rev. Med. Virol. 10 83-100. 

Rickinson AB, and Moss DJ (1997) Human cytotoxic T lymphocyte responses to Epstein-Barr virus infection. Annu. Rev. Immunol. 15 405-431. 

A viral etiology has been implicated in Burkitt s lymphoma, and there is some evidence that Epstein-Barr virus causes infectious mononucleosis in Europe and Burkitt s lymphoma in Africa. It has been suggested that if the cause of the Burkitt s lymphoma is viral, then entry of the virus particles into the lymphoid colls of the body may derange a part of the cell immune process, subsequently affecting the production of the IgM antibody, a theory which is compatible to the dysproteinemia sometimes seen in multiple myeloma and other lymphomas (N2). Also in support of this is the observation that C-reactive protein was markedly elevated in the serum of patients with Burkitt s lymphoma, and disappeared entirely from the blood when they were cured (MIO). The relationship between malarial infection and Burkitt s lymphoma has been dealt with in a previous section on malaria. 

The microenvironment may also influence apoptosis. Exposure of isolated thymocytes to TPA plus ionomycin for 24 hours enhanced apoptosis. On the other hand, when ffiymocytes were cultured in intact lobes, a 24 hour TPA plus ionomycin exposure only marginally induced apoptosis. Therefore, it appears that removing thymocytes from their thymic microenvironment makes the cells more susceptible to certain stimuli, possibly by altering their physiological status. (Moore et al., 1992). Viral infection may also alter apoptosis. Epstein-Barr virus infected human Burkitt s lymphoma cells were particularly sensitive to treatment with PdBu (42% apoptosis at 72 hours), whereas its virus free counterpart displayed only 12% apoptosis (Ishii and Gobe, 1993). 

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