Prevention of Infection-Related Cancers

2017 ◽  
Author(s):  
Marc Bulterys ◽  
Julia Brotherton ◽  
Ding-Shinn Chen
Keyword(s):  
Randomized Clinical Trials ◽  
Viral Infections ◽  
Prevention Measures ◽  
Barr Virus ◽  
Non Hodgkin Lymphoma ◽  
B Virus ◽  
Immunodeficiency Virus ◽  
Epstein Barr ◽  
Liver Flukes

This chapter discusses primary prevention measures that disrupt transmission of oncogenic infections. It begins by discussing vaccination against hepatitis B virus (HBV) and human papillomavirus (HPV), two major causes of cancer for which safe and effective vaccines are currently available. It briefly discusses the importance of treatment and prophylaxis against human immunodeficiency virus type 1 (HIV-1), which potentiates the virulence of other viral infections as well as directly increasing the incidence of non-Hodgkin lymphoma. It does not discuss the treatment of HBV or hepatitis C virus (HCV) infection, since these are considered in Chapters 25 and 33. Also beyond the scope of this chapter are the randomized clinical trials currently underway to assess the efficacy and feasibility of eradication of Helicobacter pylori (Chapters 24, 31), vaccination against Epstein-Barr virus (EBV) (Chapters 24, 26, 39), or the prevention of schistosomiasis and liver flukes (Chapters 24, 33, and 52).

scholarly journals Absolute Level of Epstein‐Barr Virus DNA in Human Immunodeficiency Virus Type 1 Infection Is Not Predictive of AIDS‐Related Non‐Hodgkin Lymphoma

2002 ◽  
Vol 186 (3) ◽  
pp. 405-409 ◽  
Author(s):  
Debbie van Baarle ◽  
Katja C. Wolthers ◽  
Egbert Hovenkamp ◽  
Hubert G. M. Niesters ◽  
Albert D. M. E. Osterhaus ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hodgkin Lymphoma ◽  
Human Immunodeficiency Virus Type ◽  
Epstein Barr Virus ◽  
Absolute Level ◽  
Barr Virus ◽  
Non Hodgkin Lymphoma ◽  
Immunodeficiency Virus ◽  
Epstein Barr

Acute Pharyngitis: Etiology and Diagnosis

PEDIATRICS ◽  
1996 ◽  
Vol 97 (6) ◽  
pp. 949-954
Author(s):  
Alan L. Bisno
Keyword(s):  
Herpes Simplex ◽  
Influenza A ◽  
Epstein Barr Virus ◽  
Viral Infections ◽  
Clinical Manifestations ◽  
Acute Pharyngitis ◽  
Herpesvirus Type ◽  
Barr Virus ◽  
Epstein Barr

Acute pharyngitis may be caused by a wide variety of microbial agents (Table 1). The relative importance of each of these agents varies greatly depending on a number of epidemiologic factors, including age of the patient, season of the year, and geographic locale. Viruses Most cases of acute pharyngitis are viral in etiology and involve the pharynx as well as other portions of the respiratory tract as manifestations of the common cold, influenza, or croup. Examples include the rhinoviruses, coronaviruses, influenza A and B, and the parainfluenza viruses. Certain viral infections causing sore throat may exhibit clinical manifestations that are rather distinctive. Examples include enteroviruses (herpangina due to Coxsackie A), Epstein-Barr virus (infectious mononucleosis), cytomegalovirus (cytomegalovirus mononucleosis), adenovirus (pharyngoconjunctival fever, acute respiratory disease of military recruits), and herpes simplex virus (pharyngitis, gingivitis, and stomatitis). In many instances, however, the illnesses caused by these agents may overlap so broadly with that of streptococcal pharyngitis as to be clinically indistinguishable. Thus, Epstein-Barr virus, adenovirus, and herpes virus may all cause fever, exudative pharyngitis, and cervical adenitis. Several studies have documented the role of primary herpesvirus type 1 infection as a cause of acute pharyngitis in college students.1-4 Herpesvirus type 2 can occasionally cause a similar illness as a consequence of oral-genital sexual contact.5 Although herpesvirus infections may involve the anterior oral cavity (vesicular or ulcerative gingivostomatitis) as well as the posterior pharynx, they do not routinely do so. Only about one-fourth of students with culturally and serologically proven primary herpes simplex type 1 pharyngitis studied by Glezen et al,2 for example, had gingivostomatitis.

scholarly journals Pancytopenia Secondary to SARS-CoV 2 Infection-A Case Reprt

2021 ◽  
Author(s):  
Neeraj Sharma ◽  
Rajat Shukla ◽  
Rachna Warrier ◽  
Kunal Kumar ◽  
Nalin Singh ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Blood Cells ◽  
Epstein Barr Virus ◽  
Viral Infections ◽  
Parvovirus B19 ◽  
Rare Complication ◽  
Elderly Male ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Epstein Barr

Abstract Pancytopenia is a condition when person has low count of all three types of blood cells causing a triage of anemia, leukopenia and thrombocytopenia. It should not be considered as a disease in itself but rather the sign of a disease that needs to be further evaluated. Among the various causes, viral infections like Human Immunodeficiency Virus, Cytomegalovirus, Epstein-Barr virus and Parvovirus B19 have been implicated. Pancytopenia is a rare complication and not commonly seen in patients with COVID 19 disease. Here, we report a case of pancytopenia in previously immunocompetent elderly male patient with SARS-CoV2 infection.

scholarly journals Profound CD4+ T lymphocytopenia in human immunodeficiency virus negative individuals, improved with anti-human herpes virus treatment

2012 ◽  
pp. 305-311 ◽  
Author(s):  
María Lilia Diaz Betancourth ◽  
Julio Cesar Klinger ◽  
Victoria Eugenia Niño
Keyword(s):  
Human Immunodeficiency Virus ◽  
Epstein Barr Virus ◽  
Herpes Virus ◽  
Viral Infections ◽  
Human Herpes ◽  
Barr Virus ◽  
Human Herpes Virus ◽  
Immunodeficiency Virus ◽  
Epstein Barr ◽  
Herpès Virus

Lymphocytopenia and CD4+ T lymphocytopenia can be associated with many bacterial, fungal, parasite and viral infections. They can also be found in autoimmune and neoplastic diseases, common variable immu­nodeficiency syndrome, physical, psychological and traumatic stress, malnutrition and immunosuppressive therapy. Besides, they can also be brought into relation, without a known cause, with idiopathic CD4+ T lym­phocytopenia. Among viral infections, the Retrovirus, specially the human immunodeficiency virus, is the most frequently cause. However, many acute viral infections, including cytomegalovirus and Epstein Barr virus can be associated with transient lymphocytopenia and CD4+ T lymphocytopenia. As is well known, transient lymphocytopenia and CD4+ T lymphocytopenia are temporary and overcome when the disease improves. Nonetheless, severe CD4+ T Lymphocytopenia associated with chronic infections by human herpes virus has not been reported. We describe 6 cases of human immunodeficiency virus negative patients, with chronic cytomegalovirus and Epstein Barr virus infections and profound lymphocytopenia with clinical symptoms of cellular immunodeficiency. These patients improved rapidly with ganciclovir or valganciclovir treatment. We claim here that it is important to consider the chronic human herpes virus infection in the differential diag­nosis of profoundly CD4+ T lymphocytopenia etiology, when human immunodeficiency virus is absent, in order to start effective treatment and to determine, in future studies, the impact of chronic human herpes virus infection in human beings’ health.

Select Viruses in Adults

2012 ◽  
pp. 61-79
Author(s):  
Randall C. Walker
Keyword(s):  
Viral Infections ◽  
Parvovirus B19 ◽  
Systemic Disease ◽  
Diagnostic Tools ◽  
Varicella Zoster ◽  
Epidemiologic Factors ◽  
Barr Virus ◽  
Epstein Barr ◽  
Simplex Virus

The following types of viral infections are discussed in this chapter: viral infections that have the capacity for multiorgan or systemic disease; infections that affect adults who may be otherwise healthy or at least not in special populations such as herpes simplex virus (HSV) type 1, varicella-zoster virus (VZV), Epstein-Barr virus, adenovirus, mumps virus, human parvovirus B19, and coxsackievirus. Reviews of these viruses focus on differentiating clinical features, diagnostic tools and treatment, and salient microbiologic and epidemiologic factors.

scholarly journals Relapse of Plasmablastic Lymphoma With Cutaneous Involvement in an Immunocompetent Male

2020 ◽  
pp. 014556132095219
Author(s):  
Samantha Shwe ◽  
Aditi A. Sharma ◽  
Bonnie A. Lee ◽  
Janellen E. Smith
Keyword(s):  
Nasal Cavity ◽  
Epstein Barr Virus ◽  
Recurrent Disease ◽  
Excisional Biopsy ◽  
Plasmablastic Lymphoma ◽  
Rare Type ◽  
Barr Virus ◽  
Non Hodgkin Lymphoma ◽  
Immunodeficiency Virus ◽  
Epstein Barr

Plasmablastic lymphoma (PBL) is a rare type of non-Hodgkin lymphoma frequently found in the context of immunosuppression and infection with human immunodeficiency virus (HIV) and/or Epstein-Barr virus (EBV). A 33-year-old immunocompetent male presented with recurrent episodes of epistaxis and a growing intranasal mass. Excisional biopsy of the mass revealed an immunohistochemical profile diagnostic of PBL. Upon completion of chemoradiation, he underwent a transnasal endoscopic mucosal flap tissue rearrangement to restore patency for both functional and surveillance purposes. There was no endoscopic evidence of residual or recurrent disease. However, 8 months later, he was found to have a relapse involving the skin. The nasal cavity is one of the most common sites affected by PBL. Involvement of the nasal cavity may present with symptoms of persistent epistaxis accompanied by an enlarging mass. A plasmablastic immunophenotype in combination with HIV or EBV positivity can aid diagnosis.

scholarly journals Subtypes of Epstein-Barr virus in human immunodeficiency virus- associated non-Hodgkin lymphoma

Blood ◽  
1991 ◽  
Vol 78 (11) ◽  
pp. 3004-3011 ◽  
Author(s):  
MJ Boyle ◽  
WA Sewell ◽  
TB Sculley ◽  
A Apolloni ◽  
JJ Turner ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hodgkin Lymphoma ◽  
Epstein Barr Virus ◽  
Type I ◽  
Type B ◽  
Barr Virus ◽  
Non Hodgkin Lymphoma ◽  
Immunodeficiency Virus ◽  
High Prevalence ◽  
Epstein Barr

Abstract Biopsy samples obtained from 20 patients with human immunodeficiency virus (HIV)-associated non-Hodgkin lymphoma (NHL) were assessed for evidence of Epstein-Barr virus (EBV) and HIV sequences. DNA was extracted from formalin-fixed, paraffin-embedded NHL tissue and specific viral gene sequences were sought using the polymerase chain reaction (PCR). EBV sequences were found in 10 NHL samples (50%), with five tumors showing A-type and five B-type sequences. By serologic testing, 18 of 19 patients had antibodies to EBV, with 14 patients having antibodies to A-type EBV and 11 to B-type EBV. Serology confirmed the high prevalence of type B EBV in HIV-infected patients, but was not a reliable indicator of the EBV subtype present in the lymphomas. HIV sequences were present in biopsy tissue but at a level consistent with an origin from bystander HIV-infected cells. All 20 patients were negative by enzyme-linked immunosorbent assay for antibodies to human T-cell leukemia virus-type I. The high prevalence of type B EBV in these tumors is similar to the findings in endemic Burkitt's lymphoma, where 40% of the tumors have type B viral sequences. In normal populations, type B EBV is rarely found outside the nasopharynx. These studies support the hypothesis that EBV is an important cofactor in NHL in HIV-infected persons. The finding that B- type EBV is present in 25% of HIV-associated NHL suggests that this EBV subtype may be an important human pathogen with a wider geographic distribution than originally thought.

Human immunodeficiency virus type 1 Tat protein modulates cell cycle and apoptosis in Epstein–Barr virus-immortalized B cells

2004 ◽  
Vol 295 (2) ◽  
pp. 539-548 ◽  
Author(s):  
Eva Colombrino ◽  
Elisabetta Rossi ◽  
Gianna Ballon ◽  
Liliana Terrin ◽  
Stefano Indraccolo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Human Immunodeficiency Virus ◽  
B Cells ◽  
Human Immunodeficiency Virus Type ◽  
Epstein Barr Virus ◽  
Tat Protein ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Epstein Barr

scholarly journals Quantitative analysis of the human immunodeficiency virus type 1 (HIV-1)-specific cytotoxic T lymphocyte (CTL) response at different stages of HIV-1 infection: differential CTL responses to HIV-1 and Epstein-Barr virus in late disease.

1993 ◽  
Vol 177 (2) ◽  
pp. 249-256 ◽  
Author(s):  
A Carmichael ◽  
X Jin ◽  
P Sissons ◽  
L Borysiewicz
Keyword(s):  
Structural Gene ◽  
Gene Products ◽  
Ctl Response ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Persistent Virus ◽  
Epstein Barr ◽  
Cd4 Lymphocyte ◽  
Hiv 1

Major histocompatibility complex (MHC)-restricted cytotoxic T lymphocytes (CTL) are part of the cellular immune response to human persistent virus infections. Measurements of the frequency and specificity of human immunodeficiency virus type 1 (HIV-1)-specific CTL and their variation with time may indicate their relative importance in modulating the progression of HIV-1 infection. We have used limiting dilution analysis (LDA) to derive quantitative estimates of the frequency of HIV-1-specific CTL precursors in a cross-sectional study of 23 patients at different clinical stages of HIV-1 infection and to compare these with the frequency of CTL precursors specific for another persistent virus (Epstein-Barr virus [EBV]) in the same patients. Peripheral blood mononuclear cells (PBMC) were stimulated in vitro with autologous HIV-1-infected lymphoblasts and assayed for cytotoxicity in 51Cr release assays against autologous and MHC-mismatched lymphoblastoid B cells infected with recombinant vaccinia viruses expressing the three HIV-1 structural gene products. The frequency of MHC-restricted precursors was high in asymptomatic HIV-1-infected patients (env-specific CTL precursors up to 73/10(6) PBMC; gag-specific CTL precursors up to 488/10(6) PBMC), although the relative frequency against the different structural gene products varied from patient to patient. The HIV-1-specific CTL precursor frequency was reduced in patients who had more severe (< 400/microliters) CD4+ lymphocyte depletion, while in the majority of such patients the frequency of CTL precursors against EBV was maintained at levels observed in healthy controls. Direct CTL activity in unstimulated PBMC was observed in three of nine patients but no correlation was found between the presence of an activated CTL response and the magnitude of the CTL response detected after stimulation in LDA. Thus, CTL precursors were detected against all three HIV-1 structural gene products in patients with CD4+ lymphocyte counts > 400/microliters, at frequencies that are high compared with those reported for other persistent viruses. A CTL response directed against multiple protein antigens of HIV-1 may protect the patient against epitope variation. The fact that the EBV-specific CTL precursor frequencies were maintained in advanced HIV-1 infection suggests that there may be selective impairment of the HIV-1-specific CTL response associated with disease progression.

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