Antonio Ali Perez-Maya

Prof. Dr. Antonio Ali Perez-Maya

Universidad Autónoma de Nuevo León, Facultad de Medicina.
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Research Focus & Metrics

Academic Career Length

15Years (2012-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 July 2018 in Infection, Genetics and Evolution
Verified
Journal Article
Closed access
Mariel Araceli Oyervides-MuñozMariel Araceli Oyervides-Muñoz
Mariel Araceli Oyervides-Muñoz
Antonio Ali Perez-MayaAntonio Ali Perez-Maya
Antonio Ali Perez-Maya
HRHazyadee Frecia Rodríguez-Gutiérrez
Hazyadee Frecia Rodríguez-Gutiérrez
GGGabriela Sofía Gómez-Macias
Gabriela Sofía Gómez-Macias
OFOscar Raúl Fajardo-Ramírez
Oscar Raúl Fajardo-Ramírez
Maria Lourdes Garza-RodríguezMaria Lourdes Garza-Rodríguez
Maria Lourdes Garza-Rodríguez

17 August 2022 in Journal of Neuroimmunology
Verified
Journal Article
Closed access
MSMaría Fernanda Serna-Rodríguez
María Fernanda Serna-Rodríguez
SBSofía Bernal-Vega
Sofía Bernal-Vega
JBJosé Alfonso Ontiveros-Sánchez de la Barquera
José Alfonso Ontiveros-Sánchez de la Barquera
ACAlberto Camacho
Alberto Camacho
Antonio Ali Perez-MayaAntonio Ali Perez-Maya
Antonio Ali Perez-Maya

31 March 2020 in Viruses
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Journal Article
Open access
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Mariel Araceli Oyervides-MuñozMariel Araceli Oyervides-Muñoz
Mariel Araceli Oyervides-Muñoz
Antonio Ali Perez-MayaAntonio Ali Perez-Maya
Antonio Ali Perez-Maya
Celia N Sánchez-DomínguezCelia N Sánchez-Domínguez
Celia N Sánchez-Domínguez
ABAnais Berlanga
Anais Berlanga
MAMauro Antonio-Macedo
Mauro Antonio-Macedo
Maria Lourdes Garza-RodríguezMaria Lourdes Garza-Rodríguez
Maria Lourdes Garza-Rodríguez
Persistent high-risk human papillomavirus (HR-HPV) infections play a major role in the development of invasive cervical cancer (CC), and screening for such infections is in many countries the primary method of detecting and preventing CC. HPV typing can be used for triage and risk stratification of women with atypical squamous cells of undetermined significance (ASC-US)/low-grade cervical lesions (LSIL), though the current clinical practice in Mexico is to diagnose CC or its preceding conditions mainly via histology and HR-HPV detection. Additional information regarding these HPV infections, such as viral load and co-infecting agents, might also be useful for diagnosing, predicting, and evaluating the possible consequences of the infection and of its prevention by vaccination. The goal of this follow-up hospital case study was to determine if HPV types, multiple HPV infections, and viral loads were associated with infection persistence and the cervical lesion grade. A total of 294 cervical cytology samples drawn from patients with gynecological alterations were used in this study. HPV types were identified by real-time PCR DNA analysis. A subset of HPV-positive patients was reevaluated to identify persistent infections. We identified HPV types 16, 18, and 39 as the most prevalent. One hundred five of the patients (59%) were infected with more than one type of HPV. The types of HPV associated with multiple HPV infections were 16, 18, and 39. In the follow-up samples, 38% of patients had not cleared the initially detected HPV infection, and these were considered persistent. We found here an association between multiple HPV infections and high viral loads with and infection persistence. Our findings suggest there are benefits in ascertaining viral load and multiple HPV infections status of HR-HPV infections for predicting the risk of persistence, a requirement for developing CC. These findings contribute to our understanding of HPV epidemiology and may allow screening programs to better assess the cancer-developing risks associated with individual HR-HPV infections.

24 April 2012 in Journal of Bacteriology
Verified
Journal Article
Closed access
LVLucio Vera-Cabrera
Lucio Vera-Cabrera
RORocio Ortiz-Lopez
Rocio Ortiz-Lopez
RER. Elizondo-Gonzalez
R. Elizondo-Gonzalez
Antonio Ali Perez-MayaAntonio Ali Perez-Maya
Antonio Ali Perez-Maya
JOJ. Ocampo-Candiani
J. Ocampo-Candiani
In Mexico, actinomycetoma is mainly caused by Nocardia brasiliensis, which is a soil inhabitant actinobacterium. Here, we report for the first time the draft genome of a strain isolated from a human case that has largely been found in in vitro and experimental models of actinomycetoma, N. brasiliensis HUJEG-1.

27 February 2015 in Mycoses
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Journal Article
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OCOlga Carolina
Olga Carolina
RLRafael B. R. León‐Cachón
Rafael B. R. León‐Cachón
Antonio Ali Perez-MayaAntonio Ali Perez-Maya
Antonio Ali Perez-Maya
MAMarcelino Aguirre‐Garza
Marcelino Aguirre‐Garza
MMMaría Moreno-Treviño
María Moreno-Treviño
GGGloria M. González
Gloria M. González

Verified
Journal Article
Open access
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Maria Lourdes Garza-RodríguezMaria Lourdes Garza-Rodríguez
Maria Lourdes Garza-Rodríguez
Mariel Araceli Oyervides-MuñozMariel Araceli Oyervides-Muñoz
Mariel Araceli Oyervides-Muñoz
Antonio Ali Perez-MayaAntonio Ali Perez-Maya
Antonio Ali Perez-Maya
Celia N Sánchez-DomínguezCelia N Sánchez-Domínguez
Celia N Sánchez-Domínguez
ABAnais Berlanga
Anais Berlanga
VICTOR TREVINOVICTOR TREVINO
VICTOR TREVINO
Human papillomavirus (HPV) DNA integration is a crucial event in cervical carcinogenesis. However, scarce studies have focused on studying HPV integration (HPVint) in early-stage cervical lesions. Using HPV capture followed by sequencing, we investigated HPVint in pre-tumor cervical lesions. Employing a novel pipeline, we analyzed reads containing direct evidence of the integration breakpoint. We observed multiple HPV infections in most of the samples (92%) with a median integration rate of 0.06% relative to HPV mapped reads corresponding to two or more sequence breakages. Unlike cancer studies, most integrations events were unique (supported by one read), consistent with the lack of clonal selection. Congruent to other studies, we found that breakpoints could occur, practically, in any part of the viral genome. We noted that L1 had a higher frequency of rupture integration (25%). Based on host genome integration frequencies, we found previously reported integration sites in cancer for genes like FHIT, CSMD1, and LRP1B and putatively many new ones such as those exemplified in CSMD3, ROBO2, and SETD3. Similar host integrations regions and genes were observed in diverse HPV types within many genes and even equivalent integration positions in different samples and HPV types. Interestingly, we noted an enrichment of integrations in most centromeres, suggesting a possible mechanism where HPV exploits this structural machinery to facilitate integration. Supported by previous findings, overall, our analysis provides novel information and insights about HPVint.