<h4>Background</h4>Infection with high-risk types of the human papillomavirus (HPV) is known to cause cervical cancer. Cervical cancer risk varies greatly by genotype, which is therefore used in screening algorithms. An extensive amount of research has also focused on the differential pathogenicity of high-risk HPV subtypes called lineages and sublineages (respectively 1.0%-10% and 0.5%-1.0% genetic difference), albeit with inconclusive and contradictory results. Therefore, the topic is systematically reviewed for the first time to determine whether the clinical use of (sub)lineage detection is supported.<h4>Methods</h4>Three databases for health sciences (PubMed, Web of Science, and Scopus) were searched for relevant papers. Meta-analysis was performed for HPV16-positive patients with cervical cancer and healthy participants using random effects models.<h4>Results</h4>The search yielded 1535 records, and 93 papers were included after the selection process. Although some trends in disease association were detected, 46 studies did not find statistically significant differences between (sub)lineages in individuals with and without cervical disease. Additionally, the reports are heterogeneous in terms of study design and often characterized by a small sample size. The meta-analysis found odds ratios of 2.2 (95% CI = 1.49 to 3.15) for HPV16 A4; 2.1 (95% CI = 1.25 to 3.40) for HPV16 D; and 0.48 (95% CI = 0.33 to 0.68) for HPV16 A1-3 with statistically significant heterogeneity (38%-77%).<h4>Conclusion</h4>This systematic review and meta-analysis provide an overview of the high-risk types of HPV (sub)lineages and association with cervical disease. Although some (sub)lineages marginally correlate with cervical malignancy, there is great variability. Unlike genotyping, this study demonstrates insufficient association between high-risk HPV (sub)lineages and cervical malignancy for clinical use to date.

Oncogenic viruses play a pernicious role in the development of cancer, causing various tumors in humans and animals. These viruses are of public health importance in developing nations. Worldwide, about 15–20% of cancer cases are related to viral infections. About 12% of all cancers in humans are attributed to oncoviruses. However, the accurate rate of cancers attributed to oncoviruses across all animal cancers remains uncertain. In some species, such as chickens and cats, oncoviruses are responsible for approximately 80–100% of specific cancer cases. The first oncovirus reported in humans was the Epstein-Barr virus, in the case of Burkitt’s lymphoma. The Jaagsiekte sheep retrovirus was the first oncovirus to be reported in livestock. The main reported tumor viruses of veterinary importance are bovine leukemia virus, jaagsiekte sheep retrovirus, feline leukemia virus, bovine papillomavirus, equine papillomavirus, Marek’s disease virus, avian leukosis virus, and reticuloendotheliosis virus. The control of oncoviruses mainly relies on early molecular methods, such as PCR, with remaining difficulties concerning virus isolation. Moreover, the potential for viral oncogenes to integrate into host genomes underscores the challenges in diagnosis, control, and eradication. These viruses have a significant impact on veterinary health in Egypt, affecting various animal species and posing substantial economic challenges. Therefore, exploring the up-to-date situation of oncogenic viruses recorded in Egypt is essential. This review aims to elucidate the general mechanisms of viral oncogenesis, shedding light on the situation of oncoviruses of veterinary importance that circulate in Egypt, as well as their diagnosis and control.

<h4>Background</h4>Maternal infections during pregnancy may increase the risk of childhood cancer (CC) in offspring by affecting foetal immunity and genetics. Existing evidence seems inconclusive, necessitating a comprehensive review to understand this association. We aimed to evaluate the risk of various CC outcomes following prenatal exposure to different types of maternal infections.<h4>Methods</h4>We searched Medline, Web of Science, Embase, Cochrane Library, and bibliographies for relevant studies from inception to October 2025. The study protocol was registered in PROSPERO (ID:CRD42023483706). We included original human epidemiological studies that examined the association between maternal infections during pregnancy and CC with appropriate reference groups and no language restrictions. We excluded studies if they were reviews or reports, if they did not assess individual-level infection or if they used therapies for infections (e.g., antibiotics) as markers of infection exposure. Two independent reviewers extracted data and assessed methodological quality following PRISMA guidelines. Pooled estimates (ES) and 95% confidence intervals (95%CIs) were calculated using random-effect models. Heterogeneity was examined in subgroup analyses. Publication bias was evaluated using Egger's tests and Funnel plots.<h4>Results</h4>From 9284 studies identified by the search, 46 studies (39 case-control,7 cohort) with over nine million participants were included, covering 33 analyses of 12 types of infection and five CC sites. Overall, maternal infection during pregnancy was associated with increased risk of CC (ES = 1.36;95%CI,1.17-1.59). Sexually transmitted infections (STIs) were associated with increased overall CC risk (ES = 2.86;95%CI,1.88-4.33). Viral infections were also associated with increased risk of overall CC (ES = 1.43;1.18,1.74), with cytomegalovirus and rubella virus infections showing positive associations upon stratification by pathogen-type. Genitourinary tract infections (GUTIs) were associated with increased risk of leukaemia (ES = 1.49;95%CI,1.05-2.12) and solid tumours (ES = 1.60, 95%CI;1.06-2.42) and viral infections with the risk of acute lymphoblastic leukaemia (ES = 1.58;95%CI,1.15-2.18).<h4>Conclusions</h4>Maternal STIs, GUTIs, and viral infections during pregnancy are associated with increased risk of CC, with GUTIs and viral infections specifically associated with increased risk of leukaemia. Targeted prevention strategies towards specific infections during pregnancy may protect against CC. Large-scale prospective studies with precise infection assessment and stratification by pathogen-type, and mechanistic considerations are needed to deepen knowledge in this area.

The epidemiology of the feline leukemia virus (FeLV). Clustering of cases of feline lymphosarcoma (LSA) has been observed by veterinarians for many years. In 1964 it was discovered that feline LSA was caused by an oncornavirus, the feline leukemia virus (FeLV). In 1970, a simple, indirect immunoflourescent antibody (IFA) test for FeLV was developed which enabled large numbers of cats, living in their natural (household) environments, to be tested for the virus. In one study, over 2,000 cats were tested and the results showed conclusively that FeLV is a contagious agent for cats. This finding was independently confirmed by several other investigators using different testing procedures. After discovering the contagious nature of FeLV a test and removal program was devised which successfully prevents the spread of FeLV and the development of FeLV diseases in the pet cat population. There is, at present, no evidence that FeLV infects humans living with FeLV infected cats. Published in Cancer (1977)

Sheep pulmonary adenomatosis: a contagious tumour and its cause. Sheep pulmonary adenomatosis (SPA) is a contagious lung tumour that can be transmitted experimentally. Two viruses have been associated with the disease, a herpesvirus and a retrovirus. All ovine herpesviruses are related antigenically and have been isolated only from SPA tumour tissues. They do not appear to cause the tumour and their association with SPA appears to arise from reactivation of latent virus in the respiratory tract. SPA tumour tissue and lung fluid contain a retrovirus that has properties similar to those of type B and type D retroviruses. Homogenates of tumour that contain this retrovirus can transmit SPA to experimentally inoculated sheep. Various retroviruses have been cultured from such tumours. Only one of these has properties similar to that of the retrovirus detected in the tumour and it can transmit SPA experimentally. The others appear to be isolates of the non-oncogenic ovine lentivirus, maedi-visna virus, and play no part in the aetiology of SPA. Published in Cancer surveys (1987)

ABSTRACT The ovine betaretroviruses jaagsiekte sheep retrovirus (JSRV) and enzootic nasal tumor virus (ENTV) cause contagious cancers in the lungs and upper airways of sheep and goats. Oncogenic transformation assays using mouse and rat fibroblasts have localized the transforming activity to the Env proteins encoded by these viruses, which require the putative lung and breast cancer tumor suppressor hyaluronidase 2 (Hyal2) to promote virus entry into cells. These results suggested the hypothesis that the JSRV and ENTV Env proteins cause cancer by inhibiting the tumor suppressor activity of Hyal2. Consistent with this hypothesis, we show that human Hyal2 and other Hyal2 orthologs that can promote virus entry, including rat Hyal2, can suppress transformation by the Env proteins of JSRV and ENTV. Furthermore, we provide direct evidence for binding of the surface (SU) region of JSRV Env to human and rat Hyal2. However, mouse Hyal2 did not mediate entry of virions bearing JSRV or ENTV Env proteins, bound JSRV SU poorly if at all, and did not suppress transformation by the JSRV or ENTV Env proteins, indicating that mouse Hyal2 plays no role in transformation of mouse fibroblasts and that the Env proteins can transform at least some cells by a Hyal2-independent mechanism. Expression of human Hyal2 in mouse cells expressing JSRV Env caused a marked reduction in Env protein levels, indicating that human Hyal2 suppresses Env-mediated transformation in mouse cells by increasing Env degr

<h4>Background</h4>Persistent infection with high-risk human papillomavirus (HPV) types is a well-established risk factor for various malignancies, and timely vaccination of university students is a cost-effective strategy to reduce infection rates and the burden of HPV-associated consequences. Although many studies have examined HPV knowledge, vaccine acceptance, and uptake in university students, findings remain heterogeneous, and comprehensive quantitative synthesis is limited. This systematic review and meta-analysis aims to assess global estimates of university students' knowledge of HPV and its vaccine, willingness to receive the vaccine, and actual vaccination behaviors.<h4>Methods</h4>The study was reported in accordance with the Preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA) 2020 Checklist. A systematic search was conducted in PubMed, Web of Science, China Biology Medicine disc, China National Knowledge Infrastructure and Wan Fang Database for studies published from January 2006 through August 2024. Studies with quality assessment scores > 5 and published in Chinese or English were included for data extraction. Pooled prevalence estimates and 95% confidence intervals (CI) were calculated using the Freeman-Tukey double arcsine transformation. The heterogeneity statistic I-squared and corresponding p value were also reported.<h4>Results</h4>A total of 56 studies covering 184,351 university students from four continents (Asia, Africa, Europe and North America) were included. Among students, 68.3% (95% CI 56.4%-79.0%) and 53.5% (95% CI 53.0%-54.1%) were aware of HPV and HPV vaccine, respectively, with significant gaps in knowledge about HPV symptoms, cervical cancer screening methods, and optimal vaccination timing. Pooled HPV vaccination willingness was 52.9% (95% CI 44.2%-61.6%), with higher willingness observed among females and medical students. Only 10.4% (95% CI 6.1%-15.8%) had received at least 1 dose of vaccination and 12.4% (95% CI 3.0%-26.9%) had completed the full three-dose schedule. Vaccination coverage among females was 8.6% (95% CI 3.7%-15.1%), and among medical students, 7.7% (95% CI 1.3%-18.4%).<h4>Conclusions</h4>This meta-analysis found that university students exhibit limited awareness of HPV and its vaccine, with about half willing to be vaccinated. Actual vaccination rates remain low and vary widely by gender, major, time of year, and geographic regions. These findings highlight the need for targeted intervention strategies, such as precision education and cross-sector collaboration, to effectively increase HPV vaccination coverage in this population.

Cancer is caused by genetic changes leading to uncontrolled cell growth and tumor formation. The basic cause of sporadic (non-familial) cancers is DNA Cancer is caused by genetic changes leading to uncontrolled cell growth and tumor formation. The basic cause of sporadic (non-familial) cancers is DNA damage and genomic instability. A minority of cancers are due to inherited genetic mutations. Most cancers are related to environmental, lifestyle, or behavioral exposures. Cancer is generally not contagious in humans, though it can be caused by on Cancer is caused by genetic changes leading to uncontrolled cell growth and tumor formation. The basic cause of sporadic (non-familial) cancers is DNA damage and genomic instability. A minority of cancers are due to inherited genetic mutations. Most cancers are related to environmental, lifestyle, or behavioral exposures. Cancer is generally not contagious in humans, though it can be caused by oncoviruses and cancer bacteria. The term "environmental", as used by cancer researchers, refers to everything outside the body that interacts with humans. The environment is not limited to the biophysical environment (e.g. exposure to factors such as air pollution or sunlight), but also includes lifestyle and behavioral factors. Over one third of cancer deaths worldwide (and about 75–80% in the United States) are potentially avoidable by reducing exposure to known factors. Common environmental factors that contribute to cancer death include exposure to different chemical and physical agents (tobacco use accounts for 25–30% of cancer deaths), environmental pollutants, diet and obesity (30–35%), infections (15–20%), and radiation (both ionizing and non-ionizing, up to 10%). These factors act, at least partly, by altering the function of genes within cells. Typically many such genetic changes are required before cancer develops. Aging has been repeatedly and consistently regarded as an important aspect to consider when evaluating the risk factors for the development of particular cancers. Many molecular and cellular changes involved in the development of cancer accumulate during the aging process and eventually manifest as cancer.

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