Cytomegalovirus, Epstein-Barr virus, and human herpesvirus-6 infections in patients with myalgic еncephalomyelitis/chronic fatigue syndrome.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling multisystem chronic disease. The etiology and pathogenesis of ME/CFS are unknown. Infections of cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus-6 (HHV-6) are suspected as etiological agents for ME/CFS.

Antihuman Immunodeficiency Virus Type 1 (HIV-1) Activity of Rare Earth Metal Complexes of 4-Hydroxycoumarins in Cell Culture.

The cerium Ce(III), lanthanum La(III), and neodymium Nd(III) complexes with 4-hydroxy-3-(3-oxo-1-phenylbutyl)-2H-1-benzopyran-2-one (warfarin) (W) and 3,3'-benzylidenebis[4-hydroxycoumarin] (1) were synthesized and studied for the first time for cytotoxicity (on MT-2 cells) and as anti-HIV agents under acute and chronic infection. The complexes were characterized by different physicochemical methods: mass spectrometry, (1)H NMR, (13)C NMR, and IR spectroscopy. The spectra of the complexes were interpreted on the basis of comparison with the spectrum of the free ligands.

Structure-Activity Relationships of Synthetic Coumarins as HIV-1 Inhibitors.

HIV/AIDS pandemics is a serious threat to health and development of mankind, and searching for effective anti-HIV agents remains actual. Considerable progress has been made in recent years in the field of drug development against HIV. A lot of structurally different coumarins were found to display potent anti-HIV activity.

An experimental model for study of sialoglycoproteins of human immunodeficiency virus 1 epitope structures.

Sialic acid (SA) molecules located terminally on retrovirus glycoproteins (gps) play a key role in virus-cell interactions. The specificity of sialylation of Human immunodeficiency virus 1 (HIV-1) gps has not yet been studied. Looking for a convenient and reproducible experimental virus-cell model for studying the problem mentioned above we compared viral sialoglycoprotein (Sgp) patterns in H9/HTLV III B cells chronically infected with laboratory-adapted HIV-1LAI and MT-2 cells acutely infected with the same virus.