Predicting the effect of the Oregon Health Plan on Medicaid coverage for outpatients with HIV.

The Oregon Health Plan, which took effect in February 1994, extends Medicaid eligibility but limits coverage to conditions and treatments above a certain threshold on a prioritized list. Retrospective analysis was conducted on records of visits to two Oregon human immunodeficiency virus (HIV) outpatient clinics in 1991 and 1992 to determine Medicaid coverage if the plan had been operational. Of 1129 patients, 21.

Factors associated with initiation of primary medical care for HIV-infected persons.

Purpose: To examine the degree of immune dysfunction of human immunodeficiency virus (HIV)-infected patients at the time of presentation and to identify factors associated with early and late initial primary medical care for HIV infection as measured by CD4+ lymphocyte count.

Patients And Methods: Two hundred fifty-one consecutive outpatients without prior primary care for HIV infection were assessed at a municipal hospital HIV intake clinic (derivation group). Sociodemographic and clinical variables were examined for their association with CD4+ cell count on presentation in bivariate and stepwise linear regression analyses.

Sequence and mapping analyses of the herpes simplex virus DNA polymerase gene predict a C-terminal substrate binding domain.

The herpes simplex virus DNA polymerase provides an excellent model for studies of eukaryotic replicative polymerases. We report here the nucleotide sequence of the gene which encodes this enzyme. The gene includes a 3705-base-pair major open reading frame capable of encoding a Mr 136,519 polypeptide, in rough agreement with previous estimates of the size of the major polypeptide found in partially purified viral polymerase preparations.

Sensitivity of arabinosyladenine-resistant mutants of herpes simplex virus to other antiviral drugs and mapping of drug hypersensitivity mutations to the DNA polymerase locus.

Seven herpes simplex virus mutants which have been previously shown to be resistant to arabinosyladenine were examined for their sensitivities to four types of antiviral drugs. These drugs were a pyrophosphate analog, four nucleoside analogs altered in their sugar moieties, two nucleoside analogs altered in their base moieties, and one altered in both. The seven mutants exhibited five distinct phenotypes based on their sensitivities to the drugs relative to wild-type strain KOS.

Fine mapping and molecular cloning of mutations in the herpes simplex virus DNA polymerase locus.

Mutations in five phenotypically distinct mutants derived from herpes simplex virus type 1 strain KOS which lie in or near the herpes simplex virus DNA polymerase (pol) locus have been fine mapped with the aid of cloned fragments of mutant and wild-type viral DNAs to distinct restriction fragments of 1.1 kilobase pairs (kbp) or less. DNA sequences containing a mutation or mutations conferring resistance to the antiviral drugs phosphonoacetic acid, acyclovir, and arabinosyladenine of pol mutant PAAr5 have been cloned as a 27-kbp Bg+II fragment in Escherichia coli.