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Biomedical subjects

D W Archibald

Publications and source records attributed to D W Archibald.

18 recordsLinked to original sources
PubMed1995

Risk of acquiring AIDS from salivary exchange through cardiopulmonary resuscitation courses and mouth-to-mouth resuscitation.

In summary, the risk of transmission of HIV and other infectious diseases by saliva during CPR training practice is extremely low because of low infectious virus titers and properties of saliva that inhibit HIV. However, it is necessary to perform decontaminations of mannequins, by application of a suitable disinfectant and by a mechanical wipe-down with a sponge, to cleanse the external buccal area of the mannequin after contact with each CPR trainee. For health care and public safety professionals training and performance of MTM ventilation during CPR should be carried out with barrier devices such as the bag-valve-mask or face shield. Guidelines and standards of the AHA, American Red Cross, and the CDC for prevention of infection during CPR and emergency cardiac care are more fully available elsewhere. If the recommended procedures are followed, the risk of acquiring HIV from saliva during MTM should be extremely low.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Decrease of heat shock protein 27/28 with heat stress in HTLV-I-transformed cells.

We have previously reported an increase of human T-lymphotropic leukemia/lymphoma virus type I (HTLV-I) replication after heat treatment of MT-2 cells, an HTLV-I-transformed human lymphoid cell line. In this study, we investigated the effect of heat stress on the expression of Hsp27/28 in MT-2 cells. In contrast with previous studies of other cell types, a decrease of Hsp27/28 expression in MT-2 cells and an increase of Hsp70 family proteins in both MT-2 and uninfected lymphoid CEM cells were found following heat treatment at 42 degrees C. Furthermore, heat treatment resulted in an early rapid increase in the phosphorylated form of Hsp27/28 in both MT-2 and CEM cells. The results suggest that early post-translational phosphorylation of HSP27/28 could be a determinant of the ability of MT-2 cells to survive hyperthermia.

Blotting, Northern↗
PubMed1994

Loss of heterozygosity involving the APC gene in oral squamous cell carcinomas.

The tumor suppressor gene adenomatous polyposis coli has been shown to be altered in colon and esophageal cancers. Because of similar causes of oral and esophageal cancers, we investigated allelic deletion of the adenomatous polyposis coli gene in oral cancers by examining tumor cells of persons normally heterozygous at a polymorphic restriction site in adenomatous polyposis coli. Deoxyribonucleic acid was extracted from 20 formalin-fixed microdissected sections and one fresh specimen of oral squamous cell carcinomas and amplified with the use of the polymerase chain reaction. The amplified deoxyribonucleic acid was digested with Rsa I, subjected to polyacrylamide gel electrophoresis, and examined for loss of heterozygosity in adenomatous polyposis coli alleles. Samples from nine persons were homozygous for the adenomatous polyposis coli restriction site in both tumor and normal tissues and thus were uninformative. Three of the 12 samples from heterozygous persons showed loss of one adenomatous polyposis coli allele in tumor tissues. The loss of an adenomatous polyposis coli gene allele in 25% of the carcinomas examined suggests that inactivation of adenomatous polyposis coli or another neighboring gene on chromosome 5q may be involved in carcinogenesis in the oral cavity.

Adult↗
PubMed1993

Loss of heterozygosity of p53 in oral cancers demonstrated by the polymerase chain reaction.

BACKGROUND: Alterations in the tumor suppressor gene p53 are the most frequently detected genetic abnormalities in human cancers. Inactivated tumor suppressor genes, including p53, often are suggested by loss of heterozygosity (LOH) studies. p53 gene inactivation has been reported in esophageal cancers. Because the etiologic factors for esophageal and intraoral carcinomas often are the same, corresponding molecular events may occur in oral squamous cell carcinoma (SCC) development. METHODS: The authors investigated LOH of the p53 gene in DNA from 27 primary oral cancers using a polymerase chain reaction (PCR)-based restriction fragment length polymorphism assay. DNA from fixed specimens of SCC and normal tissues was isolated and amplified at two p53 gene polymorphic restriction sites. RESULTS: In heterozygous individuals, 10 of 14 (71%) intraoral SCC demonstrated loss of p53 heterozygosity at one polymorphic restriction site. Two of five carcinomas showed LOH at a second site. CONCLUSIONS: These results suggest that inactivation of p53 is involved in the development or progression of SCC of the oral cavity.

Base Sequence↗
PubMed1993

Effects of human salivas on recombinant HIV-1 proteins.

Human saliva appears to contain factors that are inhibitory to HIV-1 infectivity in vitro. We investigated the effect of incubating human whole, parotid, labial minor salivary gland and sublingual/submandibular salivas with recombinant HIV-1 envelope protein (gp160). Saliva/gp160 mixtures were run on polyacrylamide gels, transferred to nitrocellulose, and assayed for the presence of gp160 using monoclonal antibodies or HIV-1-positive sera. Incubation of the gp160 with whole saliva reduced the intensity of gp160 bands to 35% of control values. Minor salivary gland saliva reduced the band intensities to 65% of control values, while other saliva types diminished gp160 to 75% of control values. Protease inhibitors had no effect. Components of untreated whole human saliva prevent the detection of the HIV-1 envelope protein gp160 by antibodies to gp120 and gp41 in immunoblots. The results suggest that complexes between whole saliva factors and certain domains of gp160 block monoclonal antibody binding or are unable to migrate through polyacrylamide gels.

Gene Products, env↗
PubMed1991

Salivary detection of HIV-1 antibodies using recombinant HIV-1 peptides.

Salivary antibodies may play a role in the absence of HIV-1 transmission by saliva. We evaluated the presence of salivary IgG antibodies to HIV-1 using a recombinant ELISA. Whole saliva was collected from 21 HIV-1-seropositive individuals and assayed in an ELISA, ASQ (Beckman Instruments, Brea, CA), consisting of a panel of six HIV-1 recombinant peptides. Saliva samples from 20 individuals demonstrated IgG to one or more peptides and 18 to two or more peptides. Samples from 20 seropositive individuals were reactive with the gp41 peptide, whereas only 12 were reactive with the two gp120 peptides. Nineteen of twenty salivas also had detectable IgG antibodies to HIV-1 by Western blotting. The results indicate that viral-specific IgG antibodies are present in the saliva of a high percentage of HIV-infected individuals and that a recombinant peptide ELISA for saliva might be useful for the detection of HIV-1 infection.

Acquired Immunodeficiency Syndrome↗
PubMed1990

In vitro inhibition of HIV-1 infectivity by human salivas.

Inhibitory factors to human immunodeficiency virus type 1 (HIV-1) in saliva may be responsible for the infrequent isolation of virus from saliva and also may account for the marked infrequency of salivary and/or oral transmission of HIV-1. Incubation of HIV-1 with human saliva followed by addition of the mixture to susceptible cells leads to partial or complete suppression of viral replication in vitro. We investigated the inhibitory effects of whole saliva and specific glandular salivas on HIV-1 infectivity as measured by viral-induced cytopathic effects in susceptible cells. Whole saliva contained marked inhibitory activity to HIV-1, strain HTLV-IIIB, and to virus infected cells. Submandibular saliva contained inhibitory activity, but of lesser quantity. Parotid saliva demonstrated no HIV-inhibitory activity. Whole saliva also appeared to contain filterable components that were inhibitory to lymphocyte growth. Passage through a .45 micron pore-size filter eliminated the viral inhibitory activity of submandibular saliva and some of the activity in whole saliva. All salivas except parotid incubated with HIV-1 followed by filtration were inhibitory suggesting that complexing of virus with high molecular weight, submandibular mucins may play a role in viral inhibition.

Antiviral Agents↗
PubMed1990

Variation of secretory antibodies in parotid saliva to human immunodeficiency virus type 1 with HIV-1 disease stage.

The secretory immune response to pathogens of the gut-associated lymphoid tissue is often independent of the systemic response. We investigated and compared the presence of antibodies to human immunodeficiency virus type 1 (HIV-1) antigens in parotid saliva and serum by Western blotting in 22 HIV-1-infected individuals. Antibodies to the HIV-1 envelope antigen gp160 were detected in saliva samples from 21 of 22 individuals and in serum from all individuals who were classified as CDC Group II, III, or IV. Antibody titers to gp160 were approximately 3000 times higher in serum than in saliva. Antibodies to viral core antigen p24 were detected in 6 of 7 Group II individuals in saliva and in 7 of 7 in serum. Antibodies to p24 were not found in the parotid saliva, but were detected in the sera of 3 of 3 Group III and 11 of 12 Group IV patients. The absence of secretory antibodies to HIV-1 core antigen p24 was correlated with CD4+ cell counts of less than 200/mm3. The results suggest that loss of secretory anti-p24 antibodies may be an early sign of progression to higher CDC clinical stages in HIV-1-infected individuals.

Blotting, Western↗
PubMed1990

Detection of salivary immunoglobulin A antibodies to HIV-1 in infants and children.

Secretory immunoglobulin A (slgA) antibodies of non-maternal origin are present in newborns and slgA to HIV-1 antigens has been detected in infected adults. In this study we investigated the presence of HIV-1-specific IgA in saliva from 41 children (aged 1 day-46 months) born to women at risk for HIV-1 infection. Saliva samples were assayed for HIV-1 antibodies with IgA-specific Western blot. The samples from 10 out of 11 children with subsequently proven infection, including one aged 6 months, demonstrated IgA antibodies to HIV-1 envelope antigens. Samples from infants under 15 months, who were born to infected mothers and subsequently shown to be uninfected, were slgA negative. Of the 12 children with continued indeterminate HIV-1 status, eight showed neither slgA nor serologic evidence of infection and four showed slgA antibodies. HIV-1-specific slgA was detectable before the age of 15 months and may prove to be valuable in the diagnosis of HIV-1 infection in infants.

Child, Preschool↗
PubMed1990

Salivary antibodies to human immunodeficiency virus type 1 in a phase I AIDS vaccine trial.

HIV-1-specific secretory antibodies may be a desirable outcome in individuals receiving AIDS vaccines. We investigated parotid and whole saliva samples for HIV-specific antibodies collected from five volunteers who received a recombinant HIV-1 envelope glycoprotein (rgp160) vaccine. Ten healthy, adult volunteers received intramuscularly either three doses of rgp160 (40 or 80 micrograms), a hepatitis B vaccine, or a placebo on days 0, 30, and 180. Saliva samples were collected on days 0, 28, 60, 120, 194, and 270 from the volunteers. All volunteers were negative for serum HIV antibodies by ELISA (Abbott). By Western blotting, serum antibodies to envelope antigens were demonstrated in one of three individuals who received the low dose vaccine and two of two who received the high dose. Antibodies to gp160 were detected in whole saliva on day 194 from one of these individuals by Western blotting. Parotid saliva collected on all dates did not contain detectable HIV-specific antibodies. The finding of HIV-1-specific antibodies in whole saliva following vaccination may indicate that development of mucosal immunity is possible.

Blotting, Western↗
PubMed1986

Salivary antibodies as a means of detecting human T cell lymphotropic virus type III/lymphadenopathy-associated virus infection.

Of 45 individuals seropositive for human T cell lymphotropic virus type III/lymphadenopathy-associated virus, 45 were found to have detectable salivary antibodies to viral antigens by a radioimmunoprecipitation assay. The results also showed that a Western blot assay for salivary antibodies may be possible. The feasibility of a diagnostic test for human T cell lymphotropic virus type III/lymphadenopathy-associated virus not requiring venipuncture is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Antibodies to human T-lymphotropic virus type III (HTLV-III) in saliva of acquired immunodeficiency syndrome (AIDS) patients and in persons at risk for AIDS.

Whole saliva samples collected from available people at risk in Boston for infection with human T-lymphotropic virus type III (HTLV-III/LAV), from late 1984 through early 1985, were analyzed for the presence of antibodies to viral proteins. Fourteen of 20 (70%) acquired immunodeficiency syndrome (AIDS) patients and 14 of 15 (93%) AIDS-related complex (ARC) patients had salivary antibodies that reacted with the virus-encoded glycoproteins gp160 and gp120 of HTLV-III infected cells. All of the AIDS and ARC patients had serum antibodies to the same antigens. Of 20 sex partners of AIDS/ARC patients, nine (45%) showed anti-HTLV-III antibodies, and four of 18 (22%) healthy homosexual males also were positive for such antibodies. Serum and salivary antibody status were the same in these groups. A minority of those patients positive for salivary antibodies to env gene-encoded gp160 and gp120 also had salivary antibodies to gag gene-encoded proteins of 55,000, 24,000, and/or 17,000 daltons. Immunoglobulin A (IgA) class antibodies comprised the majority of the salivary antibody response. The spectrum of HTLV-III proteins detected by the salivary and serum antibodies was similar. The possibility that secretory IgA from the gut-associated lymphoid system may play a role to restrict salivary transmission of HTLV-III should be considered.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

In vitro thermal enhancement of human T-cell leukaemia/lymphoma virus type I (HTLV-I) in HTLV-I-transformed cells.

Temperature elevation constitutes a beneficial component of the host defence against viral pathogens. However, heat treatment may be detrimental to HTLV-I-infected cells by increasing virion and oncoprotein production. We investigated the effects of thermal elevation on the in vitro replication of HTLV-I (human T-cell leukaemia/lymphoma virus type I) in MT-2 cells, an HTLV-I-transformed lymphoid cell line. We found that HTLV-I replication in MT-2 cells was markedly increased as demonstrated by a nearly 2-fold increase in detection of viral p24 antigen and a 20-fold increase in reverse transcriptase activity during up to 5 h of heat treatment at 42 degrees C. The results suggest that physiologic thermal elevations may induce viral production in HTLV-I-infected individuals.

Adult↗