Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Paul V. Holland is active.

Publication


Featured researches published by Paul V. Holland.


The New England Journal of Medicine | 1975

Transfusion-associated hepatitis not due to viral hepatitis type A or B.

Stephen M. Feinstone; Albert Z. Kapikian; Robert H. Purcell; Harvey J. Alter; Paul V. Holland

Twenty-two patients who had an episode of transfusion-associated hepatitis not positive for hepatitis B antigen were examined for development of antibody to heaptitis A and B antigens, cytomegalovirus and Epstein-Barr virus. Antibody response to the 27-nm virus-like hepatitis A antigen was measured by immune electron microscopy. In none of the 22 patients studied did serologic evidence of infection with hepatitis A virus develop during the study period. Nine of the 22 patients had antibody responses to cytomegalovirus, but it was difficult to relate these seroconversions to their hepatitis. In addition, all 22 patients had pre-existing antibody to the Epstein-Barr virus. It seems likely that at least a proportion of such antigen-negative transfusion-associated hepatitis is caused by other infectious agents, not yet identified.


The New England Journal of Medicine | 1976

Type B hepatitis: the infectivity of blood positive for e antigen and DNA polymerase after accidental needlestick exposure.

Harvey J. Alter; Leonard B. Seeff; Paul M. Kaplan; Vincent J. McAuliffe; Elizabeth C. Wright; John L. Gerin; Robert H. Purcell; Paul V. Holland; Hyman J. Zimmerman

To determine the relation between the presence of donor DNA polymerase and e antigen, and recipient hepatitis, we tested, under code, serums from a controlled trial of hepatitis B immune globulin used to treat individuals accidentally inoculated with HBs Ag-positive blood. All recipients lacked antibody to HBs Ag. In 29 of 31 donors, both polymerase and e were in perfect agreement; both demonstrated a highly significant correlation with recipient hepatitis (P less than 0.001). DNA polymerase/e-negative blood did not cause hepatitis. Blood containing polymerase or e antigen did not cause hepatitis in six of 31 and four of 18 recipients, respectively. Hepatitis did not correlate with transaminase or duration of antigenemia in the donor. Polymerase and e appear to be indicators of the relative infectivity of HBs Ag-positive serum, particularly after small-volume exposure. They may be important determinants in assessing infectivity of chronic carriers of HBs Ag and in evaluating efficacy of hepatitis B immune globulin and hepatitis B vaccines.


Annals of Internal Medicine | 1986

Antibody to Hepatitis B Core Antigen as a Paradoxical Marker for Non-A, Non-B Hepatitis Agents in Donated Blood

Deloris E. Koziol; Paul V. Holland; David W. Alling; Jacqueline C. Melpolder; Rachel Solomon; Robert H. Purcell; Lenita M. Hudson; Frances J. Shoup; Henry Krakauer; Harvey J. Alter

The relationship between the presence of antibody to hepatitis B core antigen (anti-HBc) in donor blood and the development of hepatitis in recipients of that blood was studied in 6293 blood donors and 481 recipients who were followed for 6 to 9 months after transfusion. Of 193 recipients of at least 1 unit of blood positive for anti-HBc, 23 (11.9%) developed non-A, non-B hepatitis compared with 12 (4.2%) of 288 recipients of only anti-HBc-negative blood (p less than 0.001). Donor anti-HBc status was not significantly associated with the development of hepatitis B in the recipient and was negatively associated with the development of cytomegalovirus hepatitis. The relationship of donor anti-HBc status and the development of non-A, non-B hepatitis in the recipient was independent of transfusion volume and elevated donor transaminase level. Although 88% of anti-HBc-positive blood units were not associated with recipient non-A, non-B hepatitis, calculation of maximal corrected efficacy predicted that exclusion of anti-HBc-positive donors might have prevented 43% of the cases of non-A, non-B hepatitis with a donor loss of 4%. Because of the serious chronic consequences of non-A, non-B hepatitis, surrogate tests for non-A, non-B virus carriers must be seriously considered.


Annals of Internal Medicine | 1972

Posttransfusion Hepatitis After Exclusion of Commercial and Hepatitis-B Antigen-Positive Donors

Harvey J. Alter; Paul V. Holland; Robert H. Purcell; Jerrold J. Lander; Stephen M. Feinstone; Andrew G. Morrow; Paul J. Schmidt

Abstract In a prospective study the exclusion of commercial blood donors and donors positive for hepatitis-B antigen (HBAg) resulted in a hepatitis frequency of only 3.7 cases/1000 units transfused...


Transfusion | 2001

HLA class II antibodies in transfusion‐related acute lung injury

Patricia M. Kopko; Mark A. Popovsky; Malcolm R. MacKenzie; Teresa Paglieroni; Kathryn N. Muto; Paul V. Holland

BACKGROUND: Transfusion‐related acute lung injury (TRALI) is a serious, sometimes fatal, complication of transfusion. Granulocyte and HLA class I antibodies present in blood donors have been associated with TRALI. HLA class II antibodies have recently been described in a few cases of TRALI.


Transfusion | 2003

TRALI: correlation of antigen-antibody and monocyte activation in donor-recipient pairs.

Patricia M. Kopko; Teresa Paglieroni; Mark A. Popovsky; Kathryn N. Muto; Malcolm R. MacKenzie; Paul V. Holland

BACKGROUND : TRALI may be a severe reaction associated with transfusion of plasma‐containing blood components. TRALI has usually been associated with antibodies against granulocytes and HLA class I antigens, but more recently with antibodies against HLA class II and monocytes. TRALI cases were investigated to determine correlation between antigen and antibody. Additionally, activation of monocytes by TRALI serums was studied.


Annals of Internal Medicine | 1990

The Prevalence of Hepatitis C Virus Antibodies among Hemodialysis Patients

Jerome B. Zeldis; Thomas A. Depner; I.K. Kuramoto; Robert G. Gish; Paul V. Holland

Excerpt The incidence of viral hepatitis in hemodialysis units has declined over the past 20 years with improved infection control strategies, including patient surveillance and segregation, plus i...


British Journal of Haematology | 1999

Transfusion-related acute lung injury

Patricia M. Kopko; Paul V. Holland

A 77-year-old man was diagnosed with acute lymphoblastic leukaemia and started induction chemotherapy with vincristine, daunorubicin and prednisolone. His haemoglobin was 7Æ1 g/dl, total white cell count 2Æ1 · 10/l and platelet count 14 · 10/l, so he was given his first transfusion of a single pool of apheresis platelets. One hour after platelet-transfusion, he became acutely unwell with severe shortness of breath. On physical examination, he had become hypotensive (blood pressure 68/40 mmHg) with tachycardia (heart rate 120 beats/ min) and tachypnoea (respiratory rate 30 breaths/min), but remained apyrexial. There was no evidence of volume-overload but lung ausculatation revealed bilateral crepitations to the midzones. The oxygen saturation in room air was 67% and a chest X-ray showed extensive pulmonary oedema (left) in comparison with his X-ray on admission (right). His clinical condition deteriorated rapidly and he died from cardiac arrest. There was no previous history of cardiovascular or respiratory disease and postmortem examination showed gross pulmonary oedema, but no significant coronary artery disease or evidence of recent myocardial ischaemia. The transfused platelets were an apheresis pool from a female donor. She was subsequently found to have anti-human leucocyte antigen class I immunoglobulin G antibodies and was retired from the donor panel. Transfusion-related acute lung injury remains an important cause of transfusion-related morbidity and mortality and should be considered in the differential diagnosis when a patient becomes acutely unwell in the first 24 h following transfusion with plasma-containing blood products.


Transfusion | 1992

Increased detection of hepatitis C virus (HCV)‐infected blood donors by a multiple‐antigen HCV enzyme immunoassay

S. Kleinman; Harvey J. Alter; Michael P. Busch; Paul V. Holland; G. Tegtmeier; M. Nelles; S. Lee; E. Page; J. Wilber; A. Polito

A new, multiple‐antigen enzyme immunoassay (EIA‐2) for hepatitis C virus (HCV) antibodies was evaluated in parallel with the previously available c100‐3 HCV EIA (EIA‐1) in 14,068 volunteer blood donors as well as in 25 cases of transfusion‐associated hepatitis C for which recipient and donor samples were available. When compared to EIA‐1, the EIA‐2 was more sensitive in detecting HCV‐infected blood donors. The EIA‐2 detected an additional 1 in 1000 EIA‐1‐negative, surrogate marker‐ negative donors who were infected with HCV as demonstrated by polymerase chain reaction (PCR). The specificity of the EIA‐2 was comparable to that of the EIA‐1, but the two tests appear to detect different populations of false‐positive donors. Recombinant immunoblot assay‐indeterminate donors were detected five times more frequently by the EIA‐2; PCR demonstrated that 21 percent of these donors were infected with HCV. The greater sensitivity of EIA‐2 was also found in 25 transfusion recipients with non‐A, non‐B hepatitis; however, in 16 percent of these cases of posttransfusion HCV infection, the EIA‐2 failed to detect an HCV‐seropositive donor. These data indicate that EIA‐2 testing will significantly reduce, but probably not eliminate, the risk of transfusion‐associated HCV infection; we estimate this residual per‐unit risk to be 1 in 2000 to 1 in 6000 units transfused. On a national level, it is projected that the replacement of the anti‐ HCV EIA‐1 with the EIA‐2 will initially prevent up to 40 additional cases of transfusion‐associated hepatitis C per day.


The Journal of Infectious Diseases | 1997

Prevalence of and Risk Factors for Antibody to Hepatitis E Virus Seroreactivity among Blood Donors in Northern California

Eric E. Mast; I. Ken Kuramoto; Michael O. Favorov; Vangie R. Schoening; Brent T. Burkholder; Craig N. Shapiro; Paul V. Holland

To evaluate antibody to hepatitis E virus (anti-HEV) seroreactivity, 5000 US blood donors were tested for anti-HEV by two EIAs: a mosaic protein assay (MPr-EIA) and a recombinant protein assay (RPr-EIA). Overall, 59 (1.2%) were seroreactive by MPr-EIA and 70 (1.4%) were seroreactive by RPr-EIA. The overall concordance between tests was 98.5% (4925/5000); the concordance among reactive sera by either test was only 27% (27/102). In a case-control study, seroreactive persons were more likely than seronegative persons to have traveled to countries in which HEV is endemic (odds ratio [OR] for MPr-EIA = 4.3, P < .001; OR for RPr-EIA = 2.5, P = .005), but 31% of MPr-EIA anti-HEV-reactive persons and 38% of RPr-EIA anti-HEV-reactive persons had no history of international travel. These findings suggest that travelers to regions in which HEV is endemic can acquire subclinical HEV infection. The significance of anti-HEV seroreactivity among persons without an international travel history needs to be determined.

Collaboration


Dive into the Paul V. Holland's collaboration.

Top Co-Authors

Avatar

Harvey J. Alter

National Institutes of Health

View shared research outputs
Top Co-Authors

Avatar

Robert H. Purcell

National Institutes of Health

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Michael P. Busch

Systems Research Institute

View shared research outputs
Top Co-Authors

Avatar

John L. Gerin

Georgetown University Medical Center

View shared research outputs
Top Co-Authors

Avatar

Kim Janatpour

University of California

View shared research outputs
Top Co-Authors

Avatar

Leonor P. Fernando

Gulf Coast Regional Blood Center

View shared research outputs
Top Co-Authors

Avatar

Denis M. Dwyre

University of California

View shared research outputs
Top Co-Authors

Avatar

Paul J. Schmidt

National Institutes of Health

View shared research outputs
Researchain Logo
Decentralizing Knowledge