Dr. Hugo Lopez-Gatell is a Mexican physician, specialist in Internal Medicine, and Master in Medical Sciences. He earned the degree of Doctor of Philosophy at the Department of Epidemiology of The Johns Hopkins Bloomberg School of Public Health.
Dr. Lopez-Gatell is currently Director of Innovation on Infectious Disease Surveillance and Control at the National Institute of Public Health in Cuernavaca, Mexico.
Before, he was Assistant Director General of Epidemiology at the Mexican Ministry of Health (2008 - 2012). In this capacity, Dr. Lopez-Gatell led the National Epidemiologic Surveillance System in Mexico and served as the National Focal Point for the International Health Regulations. He also was Deputy Director for Clinical Research, Attending Clinician at the Department of Medicine, and Consulting Clinician of the Traveller Medicine Clinic all at The National Institute of Medical Sciences and Nutrition, in Mexico City.
He has been Assistant Professor of Epidemiology at Division of Postgraduate Studies of the School of Medicine and Professor of the Residency in Epidemiology of the National Autonomous University. Since 2007, Dr. López-Gatell is member of the National System of Researchers in Mexico.
Besides his academic and public health positions he was member of the Commission of Health of the Ibero-American Program for Science and Technology (CYTED, 2008 - 2010) and since 2007 he is Member of the Board of Directors of Migrant Clinicians, Inc.
Industry Expertise (3)
Areas of Expertise (3)
- National System of Researchers, Mexico: Member
- Board of Directors of Migrant Clinicians: Member
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Gerardo Chowell, Ph.D., Stefano M. Bertozzi, M.D., Ph.D., M. Arantxa Colchero, Ph.D., Hugo Lopez-Gatell, M.D., Ph.D., Celia Alpuche-Aranda, M.D., Ph.D., Mauricio Hernandez, M.D., Ph.D., and Mark A. Miller, M.D.
In the spring of 2009, an outbreak of severe pneumonia was reported in conjunction with the concurrent isolation of a novel swine-origin influenza A (H1N1) virus (S-OIV), widely known as swine flu, in Mexico. Influenza A (H1N1) subtype viruses have rarely predominated since the 1957 pandemic. The analysis of epidemic pneumonia in the absence of routine diagnostic tests can provide information about risk factors for severe disease from this virus and prospects for its control.
Since its identification in April 2009, an A(H1N1) virus containing a unique combination of gene segments from both North American and Eurasian swine lineages has continued to circulate in humans. The lack of similarity between the 2009 A(H1N1) virus and its nearest relatives indicates that its gene segments have been circulating undetected for an extended period. Its low genetic diversity suggests that the introduction into humans was a single event or multiple events of similar viruses. Molecular markers predictive of adaptation to humans are not currently present in 2009 A(H1N1) viruses, suggesting that previously unrecognized molecular determinants could be responsible for the transmission among humans. Antigenically the viruses are homogeneous and similar to North American swine A(H1N1) viruses but distinct from seasonal human A(H1N1).
A novel influenza A (H1N1) virus has spread rapidly across the globe. Judging its pandemic potential is difficult with limited data, but nevertheless essential to inform appropriate health responses. By analyzing the outbreak in Mexico, early data on international spread, and viral genetic diversity, we make an early assessment of transmissibility and severity. Our estimates suggest that 23,000 (range 6000 to 32,000) individuals had been infected in Mexico by late April, giving an estimated case fatality ratio (CFR) of 0.4% (range: 0.3 to 1.8%) based on confirmed and suspected deaths reported to that time. In a community outbreak in the small community of La Gloria, Veracruz, no deaths were attributed to infection, giving an upper 95% bound on CFR of 0.6%. Thus, although substantial uncertainty remains, clinical severity appears less than that seen in the 1918 influenza pandemic but comparable with that seen in the 1957 pandemic. Clinical attack rates in children in La Gloria were twice that in adults (
This report updates a previous report on the influenza A (H1N1) outbreak in Mexico and summarizes public health actions taken to date by Mexico to monitor and control the outbreak.
Evidence regarding the effect of tuberculosis (TB) disease on progression of human immunodeficiency virus (HIV) disease is inconclusive. The authors estimated the effect of time-varying incident TB on time to acquired immunodeficiency syndrome (AIDS)-related mortality using a joint marginal structural Cox model. Between 1995 and 2002, 1,412 HIV type 1 (HIV-1)-infected women enrolled in the Women's Interagency HIV Study were followed for a median of 6 years. Twenty-nine women incurred incident TB, and 222 died of AIDS-related causes. Accounting for age, CD4 cell count, HIV-1 RNA level, serum albumin level, and non-TB AIDS at study entry, as well as for time-varying CD4 cell count, CD4 cell count nadir, HIV-1 RNA level, peak HIV-1 RNA level, serum albumin level, HIV-related symptoms, non-TB AIDS, anti-Pneumocystis jiroveci prophylaxis, antiretroviral therapy, and household income, the hazard ratio for AIDS-related death comparing time after incident TB with time before incident TB was 4.0 (95% confidence interval (CI): 1.2, 14). The effect of incident TB on mortality was similar among highly active antiretroviral therapy (HAART)-exposed women (hazard ratio = 4.3, 95% CI: 0.9, 22) and non-HAART-exposed women (hazard ratio = 3.9, 95% CI: 0.9, 17; interaction p = 0.91). Although results were imprecise because few women incurred TB, irrespective of HAART exposure, incident TB increases the hazard of AIDS-related death among HIV-infected women.