Intracellular infections

Most infected cell lines can be fixed and stained for p24 3 4 d after infection. Intracellular p24 accumulates more slowly after infection of macrophages and these cells are usually fixed 18-21 d post-infection. Cells are fixed for up to 10 min with 500 pL of cold methanol/acetone (1 1). 

Cell membranes are complex dynamical structures primarily consisting of a bilayer in which two layers of phospholipid molecules are arranged in a way that the hydrophilic heads shield the hydrophobic lipid tails from the water [1-3]. As a permeability barrier, the membrane can protect the cell from the environment and maintain membrane protein stability and function [1-3]. Many cellular processes such as endocytosis, exocytosis, fertilization, signal transduction, viral infection, intracellular transport, and cell aggregation are mediated by such a biomembrane [4]. For example, membrane fusion, a ubiquitous life process, is generally controlled by the fusion proteins inserted in the core of cell membrane [5,6]. Probably... 

Vimses are obligate intracellular parasites. They only exhibit activity by infecting other living organisms, thus they are not a practical concern in industrial microbiological fields. The exception is where viral contamination of the product or process represents a threat of transmission of disease. Microscopic insects and protozoans are also not addressed in this article (see Insectcontroltechnology). 

The mechanism of inhibition has not been characterized, but it is probably related to the ionophoretic properties of these antibiotics. Monensin has been shown to inhibit the intracellular transport of viral membrane proteins of cells infected with Semliki Forest vims (169). The formation of syncytia, normally observed when T-lymphoblastoid cell line (CEM) cells are cocultivated with human immunodeficiency vims (HlV-l)-infected T-ceU leukemia cell line (MOLT-3) cells, was significantly inhibited in the presence of monensin (170). This observation suggests that the viral glycoproteins in the treated cells were not transported to the cell surface from the Golgi membrane. 

Infection with the obligatory intracellular parasite T. gondii is mainly acquired by ingestion of contaminated food or water. Approximately a third of the world s human population is infected. 

Furthermore, the inability of the drug to reach the focus of the infection or to reach bacteria with intracellular location may be a common reason for the failure of antibiotic treatment. 

Yamamoto M, Hayashi N, Takehara T, Ueda K, Mita E, Tatsumi T, Sasaki Y, Kasahara A, Hori M (1999) Intracellular single-chain antibody against hepatitis B virus core protein inhibits the replication of hepatitis B virus in cultured cells. Hepatology 30 300-307 Yang 00, Tran AC, Kalams SA, Johnson RP, Roberts MR, Walker BD (1997) Lysis of HIV-1-infected cells and inhibition of viral replication by universal receptor T cells, Proc Natl Acad Sci USA 94 11478-11483... 

Blum AS, Dal Pan GJ et al (1996) Low-dose zalcitabine-related toxic neuropathy frequency, natural history, and risk factors. Neurology 46(4) 999-1003 Bradley WG, Verma A (1996) Painful vascuhtic neuropathy in HlV-1 infection relief of pain with prednisone therapy. Neurology 47(6) 1446-1451 Breen EC (2002) Pro- and anti-inflammatory cytokines in human immunodeficiency virus infection and acquired immunodeficiency syndrome. Pharmacol Ther 95(3) 295-304 Bremer J (1990) The role of carnitine in intracellular metabolism. J Clin Chem Clin Biochem 28(5) 297-301... 

In some infections the pathogenic organisms are located intracellularly within phagocytic cells and, therefore, remain relatively protected from drugs which penetrate cells poorly, such as the penicillins and cephalosporins. In contrast, erythromycin, rifampicin and chloramphenicol readily penetrate phagocytic cells. Legionnaires disease is an example of an intracellular infection and is treated with rifampicin and/or erythromycin. 

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