We report a case of reinfection by SARS-CoV-2 with the second virus harboring amino acid changes in the Spike protein (141-143del, D215A, ins215AGY, L452R, D614 G), orf1a, helicase, orf3a, and Nucleocapside. The virus associated with the reinfection, from an endemic lineage containing the S:L452R immune escape mutation, was circulating in Panama at the time.

Background: Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infections and hospitalization in infants and children. Whole genome sequencing (WGS) plays a critical role in understanding the evolution and epidemiology of RSV. Limited studies have been conducted in Central America and the Caribbean, and none have specifically focused on lineages involved in recent outbreaks. Furthermore, no assays currently exist to evaluate the sensitivity of the RSV fusion protein to monoclonal antibodies. Methods: In Panama, an epidemiological surveillance system tracks RSV activity through the collection of nasopharyngeal samples from patients with acute respiratory infections. Between January 2018 and July 2024, 303 RSV‐positive samples were analyzed by RT‐qPCR. RSV‐B was the dominant subgroup in 2018, but following years had alternating dominance between RSV‐A and RSV‐B. Of the 303 samples, 115 underwent WGS. Additionally, neutralization assays were done using different Anti‐F Monoclonal Antibodies. Results: In RSV‐A, 11 lineages were identified, with 3 to 5 cocirculating during each annual outbreak, and a shift in predominance from A.D .1 (2019) to A.D .5.2 (2023–2024). In RSV‐B, two lineages circulated: B.D.4.1.1 (2018–2020) and its descendant B.D.E.1, which predominated from 2021 onward. Several monoclonal antibodies, including nirsevimab's precursor MEDI8897*, effectively neutralized the RSV strains in neutralization assays. Conclusions: Although Panama has not yet implemented a preventive therapy for RSV, this step could modify outbreak dynamics. The findings from this study provide a baseline reference prior to the implementation of preventive therapies against RSV in Panama and the region, facilitating the assessment of potential changes in the evolutionary dynamics of the virus.

Most of the information on clinical factors related to HIV infection is focused on key populations and young people. Therefore, there is little information on clinical factors related to HIV infection in older persons (>45 years old). In this study, data on CD4 lymphocyte counts were analyzed on adults who are linked to care and have their first CD4 cell count done from different regions of the Republic of Panama from 2012 to 2017. Samples were grouped according to late presentation status, region of origin in the country, year, gender, and age groups. Factors associated with late presentation to care and advanced HIV were assessed on each group by multivariable logistic regression. Late presentation to care was observed in 71.6% of the evaluated subjects, and advanced HIV in 54.5%. Late presentation was associated with males (adjusted odds ratio [AOR] = 1.3, 95% confidence interval [CI]=1.1–1.6, p = 0.03), age greater than 45 years old (AOR = 2.3 CI= 1.8–2.9, p < 0.001), and being from regions where antiretroviral clinics are not well instituted (AOR = 2.1, CI = 1.6–2.7, p < 0.001). Despite an increase in subjects linked to care with a CD4 test performed over the years, late presentation remained constant. Therefore, prevention policies must be reformulated. Promotion of routine HIV testing, accessibility among all population groups, installation of antiretroviral clinics, and implementation of programs as rapid initiation of antiretroviral therapy should be rolled out nationally.

There is limited evidence regarding severe acute respiratory syndrome coronavirus 2 infection in the placenta of pregnant women who tested positive, and if this could be a route for vertical transmission of the virus in utero. We present the cases of 2 pregnant women in their third trimester who were admitted for delivery by cesarean delivery and who, through universal screening, tested positive for coronavirus disease 2019. The maternal and fetal sides of the placenta were sectioned from both patients for viral analysis. Real-time polymerase chain reaction analysis of the placental-extracted RNA revealed a severe acute respiratory syndrome coronavirus 2 infection on the fetal side of the placenta in both patients. The virus was isolated from the patient with the lowest cycle threshold value on the fetal side of the placenta. Whole genome sequencing showed that the virus detected in this placenta was from the B1 lineage. Immunohistochemical analysis of the placental tissue detected severe acute respiratory syndrome coronavirus 2 in the endothelial cells of chorionic villi vessels proximal to both the maternal and fetal sides, with a granular cytoplasmic pattern and perinuclear reinforcement. Histologic examination of the placenta also detected a dense infiltrate of lymphoid cells around decidual vessels and endothelial cells with cytopathic changes, especially on the maternal side. Nasopharyngeal swabs from the infants that were subjected to reverse transcription quantitative polymerase chain reaction testing were negative for severe acute respiratory syndrome coronavirus 2 at 24 hours after birth. A follow-up analysis of the infants for immunoglobin G and immunoglobin M expression, clinical manifestations, and long-term developmental abnormalities is recommended.

Low-frequency mutations associated with drug resistance have been related to virologic failure in subjects with no history of pre-treatment and recent HIV diagnosis. In total, 78 antiretroviral treatment (ART)-naïve subjects with a recent HIV diagnosis were selected and followed by CD4+ T lymphocytes and viral load tests to detect virologic failure. We sequenced the basal samples retrospectively using next-generation sequencing (NGS), looking for low-frequency mutations that had not been detected before using the Sanger sequencing method (SSM) and describing the response to ART. Twenty-two subjects developed virologic failure (VF), and thirteen of them had at least one drug-resistance mutation associated with Reverse Transcriptase Inhibitors (RTI) and Protease Inhibitors (PIs) at frequency levels ≤ 1%, not detected previously in their basal genotyping test. No resistance mutations were observed to Integrase Strand Transfer Inhibitors (INSTIs). We identified a possible cause of VF in ART-naïve subjects with low-frequency mutations detected. To our knowledge, this is the first evaluation of pre-existing drug resistance for HIV-1 minority variants carried out on ART-naïve people living with HIV/AIDS (PLWHA) by analyzing the HIV-1 pol gene using NGS in the country.