PERILOUS HIV BRINGS OUT DEADLY CANCERS

2020 ◽  
pp. 1-5
Author(s):  
Camila A Carlman ◽  
Bharat Mishra ◽  
Anita Patel
Keyword(s):  
Immune System ◽  
Hodgkin Lymphoma ◽  
Cancer Progression ◽  
Kaposi's Sarcoma ◽  
Cellular Proliferation ◽  
Kaposi’S Sarcoma ◽  
Hiv Patients ◽  
Non Hodgkin Lymphoma ◽  
Increased Risk ◽  
Risk Of Cancer

Human Immunodeficiency Virus (HIV) infection is both infectious and contagious disease. The people infected with HIV have an increased risk of cancer while comparing with uninfected people. Kaposi’s sarcoma, aggressive B-cell Non-Hodgkin Lymphoma & cervical cancer are the three types of cancers which are termed as “HIV –associated cancers”. Apart from these cancers, HIV patients are prone to cancers of anus, liver, lung, pharynx which are termed as “non-AIDS defining cancers”. Viral oncogenesis and cytokine induced growth contribute to the development of Kaposi sarcoma. Several virally encoded genes such as bcl-2, IL-6, cyclin-D, GPCR & interferon regulatory factor, plays key role in cellular proliferation and survival.  Infection with HIV weakens the immune system and reduces the body’s ability to fight against viral infections that may lead to cancer. Immunosuppression and inflammation in HIV patients also contribute to cancer progression. The complications of AIDS- related cancers include easy bleeding and bruising, tiredness, nausea, vomiting, poor appetite, mouth sores, hair loss etc. According to the data, HIV infected males are more susceptible to Kaposi’s sarcoma and Non- Hodgkin Lymphoma whereas females are more liable to cervical cancers. Early diagnosis and treatment options help to drop the risk of AIDS related cancers. The HAART therapy reduces the risk of cancer in HIV patients by lowering the amount of HIV circulating in blood, so that function of immune system to fight against the virus can be restored. Other treatment methods are chemotherapy, immunotherapy, radiation and surgery.

scholarly journals The Cancer-Associated Virus Landscape in HIV Patients with Oral Hairy Leukoplakia, Kaposi's Sarcoma, and Non-Hodgkin Lymphoma

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Peter D. Burbelo ◽  
Joseph A. Kovacs ◽  
Jason Wagner ◽  
Ahmad Bayat ◽  
Craig S. Rhodes ◽  
...  
Keyword(s):  
Hodgkin Lymphoma ◽  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Hiv Positive ◽  
Infectious Agents ◽  
Hiv Patients ◽  
Non Hodgkin Lymphoma ◽  
Oral Hairy Leukoplakia ◽  
Hairy Leukoplakia ◽  
Antibody Levels

Although HIV-positive patients are at higher risk for developing a variety of infection-related cancers, the prevalence of infections with the seven known cancer-associated viruses has not been studied. Luciferase immunoprecipitation systems were used to evaluate antiviral antibodies in four 23-person groups: healthy blood donors and HIV-infected patients with oral hairy leukoplakia (OLP), Kaposi's sarcoma (KS), or non-Hodgkin lymphoma (NHL). Antibody profiling revealed that all HIV-positive individuals were strongly seropositive for anti-gp41 and antireverse transcriptase antibodies. However, anti-p24 HIV antibody levels were highly variable and some OLP and KS patients demonstrated weak or negative responses. Profiling two EBV antigens revealed no statistical difference in antibody levels among the three HIV-infected groups. A high frequency of KSHV infection was detected in HIV patients including 100% of KS, 78% of OLP, and 57% of NHL patients. Most HIV-infected subjects (84%) showed anti-HBV core antibodies, but only a few showed antibodies against HCV. MCV seropositivity was also common (94%) in the HIV-infected individuals and KS patients showed statistically higher antibody levels compared to the OLP and NHL patients. Overall, 68% of the HIV-infected patients showed seropositivity with at least four cancer-associated viruses. Antibody profiles against these and other infectious agents could be useful for enhancing the clinical management of HIV patients.

Risk of non-Hodgkin lymphoma and Kaposi's sarcoma in homosexual men

The Lancet ◽  
1990 ◽  
Vol 336 (8709) ◽  
pp. 248-249 ◽  
Author(s):  
CharlesS Rabkin ◽  
JamesJ Goedert
Keyword(s):  
Hodgkin Lymphoma ◽  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Homosexual Men ◽  
Non Hodgkin Lymphoma

ABV (doxorubicin [Adriamycin], bleomicin and vincristine) polychemotherapy regimen in HIV Kaposi’s Sarcoma: Uruguaian 10-year experience

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 9559-9559 ◽  
Author(s):  
G. Krygier ◽  
A. Sosa ◽  
A. Blanco ◽  
K. Lombardo ◽  
C. Castillo ◽  
...  
Keyword(s):  
Viral Load ◽  
Partial Response ◽  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Severe Toxicity ◽  
Effective Treatment Option ◽  
Hiv Patients ◽  
Non Hodgkin Lymphoma ◽  
Grade 3 ◽  
Aids Clinical Trials

9559 Background: Kaposi’s sarcoma is the most common malignancy among HIV patients and is considered to be one of the AIDS defining conditions. This abstract illustrates our 10 year experience with the treatment of 32 Kaposi’s sarcoma HIV patients with the same therapeutic approach. Methods: Between 04/95 and 03/05 we recruited 32 previously untreated patients that were diagnosed with Kaposi’s sarcoma and treated at the Servicio de Oncologia Clinica (Universitary Clinicas Hospital) in Montevideo. All of them received the same iv polychemotherapy plan (Adriamycin 10mg/m2, Bleomycin 10 U/m2 and Vincristine 1.4 mg/m2, every two weeks until tumor progression or severe toxicity). Results: 21 of the patients were good risk ones and the remaining 11 were poor risk patients (AIDS Clinical Trials Group staging classification). CD4 levels varied from 6 to 780/ml and the viral load ranges were 240 to 89000 copies. The patients received an average of 10.2 (4–21) polychemotherapy cycles. Grade 3–4 myelotoxicity was reported in 5 patients delaying the onset of the subsequent cycles. Grade 2 neurotoxicity was seen in 7 patients after 4, 5, 6, 8, 10, 11 and 13 cycles of ABV, changing vincristine for vinblastine (4mg/m2 every two weeks) in these patients. All the patients achieved a partial response with improvements in CD4 levels and viral load. 13/32 patients experienced a relapse (3–29 months after last chemotherapy cycle). 3 patients were retreated with paclitaxel 135 mg/m2 with 2/3 new partial responses of shorter duration. 5 patients received 4 additional ABV cycles achieving a new partial response. 5 patients refused further treatment dying due to progressive disease. One relapsed patient developed a second malignancy (High grade Non Hodgkin lymphoma) dying three months later. Conclusions: These data suggest that ABV regimen is still an effective treatment option for HIV-Kaposi’s sarcoma, specially in the undeveloped countries in which the cost of other better internationally approved options (liposomal doxorubicin and daunorubicin) makes them unaccesible for the majority of the population. No significant financial relationships to disclose.

scholarly journals A prospective study of serum soluble CD30 concentration and risk of non-Hodgkin lymphoma

Blood ◽  
2009 ◽  
Vol 114 (13) ◽  
pp. 2730-2732 ◽  
Author(s):  
Mark P. Purdue ◽  
Qing Lan ◽  
Otoniel Martinez-Maza ◽  
Martin M. Oken ◽  
William Hocking ◽  
...  
Keyword(s):  
B Cell ◽  
Hodgkin Lymphoma ◽  
Ovarian Cancer Screening ◽  
Hiv Patients ◽  
Cell Stimulation ◽  
Non Hodgkin Lymphoma ◽  
Soluble Cd30 ◽  
Increased Risk ◽  
A Prospective Study ◽  
Nested Case Control

Abstract Prediagnostic serum concentration of soluble CD30 (sCD30), a marker for chronic B-cell stimulation, has been associated with increased risk of developing AIDS-related non-Hodgkin lymphoma (NHL) in a recent study of HIV+ patients. To investigate among healthy persons whether serum sCD30 is associated with NHL risk, we carried out a nested case-control study within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. There was a strong dose-response relationship between prediagnostic sCD30 concentration and NHL risk among 234 cases and 234 individually matched controls (odds ratio [95% confidence interval] for second, third, and fourth quartiles vs first quartile: 1.4 [0.8-2.6], 2.2 [1.2-4.1], 4.1 [2.2-7.8]; Ptrend < .001), which persisted among cases diagnosed 6 to 10 years after providing a blood sample. Given that a similar relationship has been observed among HIV+ patients, our findings suggest that chronic B-cell stimulation may be an important mechanism involved in B-cell lymphomagenesis among severely immunocompromised and healthy populations alike.

scholarly journals Major Histocompatibility Complex Class II HLA-DRα Is Downregulated by Kaposi's Sarcoma-Associated Herpesvirus-Encoded Lytic Transactivator RTA and MARCH8

2016 ◽  
Vol 90 (18) ◽  
pp. 8047-8058 ◽  
Author(s):  
Zhiguo Sun ◽  
Hem Chandra Jha ◽  
Yong-gang Pei ◽  
Erle S. Robertson
Keyword(s):  
Major Histocompatibility Complex ◽  
Immune System ◽  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Complex Class ◽  
Transcription Activator ◽  
Mhc Ii ◽  
Histocompatibility Complex ◽  
Kaposi's Sarcoma Associated Herpesvirus ◽  
Kaposi’S Sarcoma Associated Herpesvirus

ABSTRACTKaposi's sarcoma-associated herpesvirus (KSHV) maintains two modes of life cycle, the latent and lytic phases. To evade the attack of the cell host's immune system, KSHV switches from the lytic to the latent phase, a phase in which only a few of viral proteins are expressed. The mechanism by which KSHV evades the attack of the immune system and establishes latency has not been fully understood. Major histocompatibility complex class II (MHC-II) molecules are key components of the immune system defense mechanism against viral infections. Here we report that HLA-DRα, a member of the MHC-II molecules, was downregulated by the replication and transcription activator (RTA) protein encoded by KSHV ORF50, an important regulator of the viral life cycle. RTA not only downregulated HLA-DRα at the protein level through direct binding and degradation through the proteasome pathway but also indirectly downregulated the protein level of HLA-DRα by enhancing the expression of MARCH8, a member of the membrane-associated RING-CH (MARCH) proteins. Our findings indicate that KSHV RTA facilitates evasion of the virus from the immune system through manipulation of HLA-DRα.IMPORTANCEKaposi's sarcoma-associated herpesvirus (KSHV) has a causal role in a number of human cancers, and its persistence in infected cells is controlled by the host's immune system. The mechanism by which KSHV evades an attack by the immune system has not been well understood. This work represents studies which identify a novel mechanism by which the virus can facilitate evasion of an immune system. We now show that RTA, the replication and transcription activator encoded by KSHV (ORF50), can function as an E3 ligase to degrade HLA-DRα. It can directly bind and induce degradation of HLA-DRα through the ubiquitin-proteasome degradation pathway. In addition to the direct regulation of HLA-DRα, RTA can also indirectly downregulate the level of HLA-DRα protein by upregulating transcription of MARCH8. Increased MARCH8 results in the downregulation of HLA-DRα. Furthermore, we also demonstrate that expression of HLA-DRα was impaired in KSHVde novoinfection.

scholarly journals Human papillomavirus-driven immune deviation: challenge and novel opportunity for immunotherapy

2017 ◽  
Vol 5 (3) ◽  
pp. 69-82 ◽  
Author(s):  
Sigrun Smola ◽  
Connie Trimble ◽  
Peter L. Stern
Keyword(s):  
Human Papillomavirus ◽  
Immune System ◽  
Immune Escape ◽  
Hpv Vaccination ◽  
Suppressor Cells ◽  
Clinical Problem ◽  
Hpv Infection ◽  
Treatment Protocols ◽  
Increased Risk ◽  
Risk Of Cancer

It is now recognized that the immune system can be a key component of restraint and control during the neoplastic process. Human papillomavirus (HPV)-associated cancers of the anogenital tract and oropharynx represent a significant clinical problem but there is a clear opportunity for immune targeting of the viral oncogene expression that drives cancer development. However, high-risk HPV infection of the target epithelium and the expression of the E6/E7 oncogenes can lead to early compromise of the innate immune system (loss of antigen-presenting cells) facilitating viral persistence and increased risk of cancer. In these circumstances, a succession of interacting and self-reinforcing events mediated through modulation of different immune receptors, chemokine and cytokine responses (CCL20; CCL2; CCR2; IL-6; CCR7; IL-12) further promote the generation of an immune suppressive microenvironment [increased levels of Tregs, Th17, myeloid-derived suppressor cells (MDSCs) and PD-L1]. The overexpression of E6/E7 expression also compromises the ability to repair cellular DNA, leading to genomic instability, with the acquisition of genetic changes providing for the selection of advantaged cancer cells including additional strategies for immune escape. Therapeutic vaccines targeting the HPV oncogenes have shown some encouraging success in some recent early-phase clinical trials tested in patients with HPV-associated high-grade anogenital lesions. A significant hurdle to success in more advanced disease will be the local and systemic immune suppressive factors. Interventions targeting the different immunosuppressive components can provide opportunity to release existing or generate new and effective antitumour immunity. Treatments that alter the protumour inflammatory environment including toll-like receptor stimulation, inhibition of IL-6-related pathways, immune-checkpoint inhibition, direct modulation of MDSCs, Tregs and macrophages could all be useful in combination with therapeutic HPV vaccination. Future progress in delivering successful immunotherapy will depend on the configuration of treatment protocols in an insightful and timely combination.

scholarly journals Increased risk of myelotoxicity in elderly patients with non-Hodgkin lymphoma

Cancer ◽  
2003 ◽  
Vol 100 (1) ◽  
pp. 6-11 ◽  
Author(s):  
Lodovico Balducci ◽  
Lazzaro Repetto
Keyword(s):  
Elderly Patients ◽  
Hodgkin Lymphoma ◽  
Non Hodgkin Lymphoma ◽  
Increased Risk

Lifetime physical inactivity is associated with increased risk for Hodgkin and non-Hodgkin lymphoma: A case-control study

2018 ◽  
Vol 69 ◽  
pp. 7-11 ◽  
Author(s):  
John Lewis Etter ◽  
Rikki Cannioto ◽  
Kah Teong Soh ◽  
Emad Alquassim ◽  
Hani Almohanna ◽  
...  
Keyword(s):  
Hodgkin Lymphoma ◽  
Physical Inactivity ◽  
Case Control Study ◽  
Case Control ◽  
Non Hodgkin Lymphoma ◽  
Increased Risk ◽  
Control Study

Physical Activity, Sedentary Behaviors, and Risk of Cancer

2017 ◽  
Author(s):  
Steven C. Moore ◽  
Charles E. Matthews ◽  
Sarah Keadle ◽  
Alpa V. Patel ◽  
I-Min Lee
Keyword(s):  
Physical Activity ◽  
The United States ◽  
Moderate Intensity ◽  
Activity Levels ◽  
Breast Cancers ◽  
Sedentary Behaviors ◽  
Moderate Intensity Physical Activity ◽  
Non Hodgkin Lymphoma ◽  
Increased Risk ◽  
Risk Of Cancer

Current physical activity guidelines recommend that adults perform at least 150 minutes per week of moderate-intensity physical activity (e.g., brisk walking), or 75 minutes per week of vigorous-intensity activity (e.g., jogging), or an equivalent combination of these. In the United States and worldwide, many adults fail to meet these recommended activity levels, with deleterious consequences for health, including increased risk of some cancers. This chapter reviews the epidemiologic evidence for links between physical activity and cancer, emphasizing published meta-analyses and the results of a recent large consortium-based study. The authors find the evidence to be convincing that physical activity reduces risk of colon and female breast cancers, and probable that it reduces risk of kidney and endometrial cancers. Moreover, physical activity has been associated with lower risk of cancers of the bladder, liver, gastric cardia, head and neck, esophagus (adenocarcinoma), and myeloma, myeloid leukemia, and non-Hodgkin lymphoma.

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