Ameni Sallemi
Research Subjects
Ameni Sallemi has a total of 20 co-authors. Here are the top co-authors by number of shared publications:
- Ilhem Boutiba-Ben Boubaker
Department of Microbiology, Charles Nicolle Hospital, Tunis 1006, Tunisia
2 shared publications - Abdulwahab Kammon
National Research Centre for Tropical and Transboundary Diseases, Alzintan 61053, Libya
1 shared publication - Adem Eljerbi
National Center for Disease Control, Tripoli 71171, Libya
1 shared publication - Amal Barakat
Regional Office for the Eastern Mediterranean, World Health Organization, Cairo 7608, Egypt
1 shared publication - Amal Miraoui
Pediatric Intensive Care Unit, University of Tunis of EL-Manar, Faculty of Medicine of Tunis, Children’s Hospital Bechir Hamza of Tunis, Tunis, Tunisia
1 shared publication - Haider El-Saeh
National Center for Disease Control, Tripoli 71171, Libya
1 shared publication
Latest Publications
- Open Access
- 8 May 2026
- Published by MDPI AG in Tropical Medicine and Infectious Disease
- Vol. 11 (5) , 127
Sentinel Surveillance of Influenza A in Libya: Subtyping and Genomic Analysis During Recent Seasons (2022–2024)
Influenza sentinel surveillance in Libya was formally established in 2022 by the Libyan National Center for Disease Control (NCDC). Between 2022 and 2024, a total of 1864 nasopharyngeal specimens were collected from patients presenting with influenza-like illness and tested using the GeneXpert for influenza A virus, influenza B virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and respiratory syncytial virus (RSV). Influenza A virus was detected in 21.1% (393/1864) of samples and influenza B virus was detected in 5.4% of samples (100/1864). SARS-CoV-2 and RSV were identified in 11.6% (216/1864) and 4.1% (77/1864) of specimens, respectively. A subset of 22 influenza A-positive samples was selected based on sample availability and sufficient remaining volume after the initial test for confirmatory testing and further molecular characterization. Real-time RT-PCR subtyping identified 11 A(H1N1)pdm09 and four A(H3N2) viruses. Whole-genome sequencing was successfully performed for 11 isolates, followed by phylogenetic analysis. Genetic characterization revealed that all A(H1N1)pdm09 viruses belonged to clade 6B.1A.5a.2a (5a.2a), while A(H3N2) viruses clustered within clade 3C.2a1b.2a.2a.3a.1 (2a.3a.1) were based on hemagglutinin gene mutations. No neuraminidase mutations associated with antiviral resistance were detected. This study represents the first molecular and phylogenetic characterization of circulating human influenza viruses in Libya, with sequence data submitted to the Global Initiative on Sharing All Influenza Data (GISAID) to establish baseline genetic data for influenza viruses in Libya.
- 8 May 2026
- Published by MDPI AG in Tropical Medicine and Infectious Disease
- Vol. 11 (5) , 127
Open AccessSentinel Surveillance of Influenza A in Libya: Subtyping and Genomic Analysis During Recent Seasons (2022–2024)
Influenza sentinel surveillance in Libya was formally established in 2022 by the Libyan National Center for Disease Control (NCDC). Between 2022 and 2024, a total of 1864 nasopharyngeal specimens were collected from patients presenting with influenza-like illness and tested using the GeneXpert for influenza A virus, influenza B virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and respiratory syncytial virus (RSV). Influenza A virus was detected in 21.1% (393/1864) of samples and influenza B virus was detected in 5.4% of samples (100/1864). SARS-CoV-2 and RSV were identified in 11.6% (216/1864) and 4.1% (77/1864) of specimens, respectively. A subset of 22 influenza A-positive samples was selected based on sample availability and sufficient remaining volume after the initial test for confirmatory testing and further molecular characterization. Real-time RT-PCR subtyping identified 11 A(H1N1)pdm09 and four A(H3N2) viruses. Whole-genome sequencing was successfully performed for 11 isolates, followed by phylogenetic analysis. Genetic characterization revealed that all A(H1N1)pdm09 viruses belonged to clade 6B.1A.5a.2a (5a.2a), while A(H3N2) viruses clustered within clade 3C.2a1b.2a.2a.3a.1 (2a.3a.1) were based on hemagglutinin gene mutations. No neuraminidase mutations associated with antiviral resistance were detected. This study represents the first molecular and phylogenetic characterization of circulating human influenza viruses in Libya, with sequence data submitted to the Global Initiative on Sharing All Influenza Data (GISAID) to establish baseline genetic data for influenza viruses in Libya.
- Open Access
- 30 April 2026
- Published by MDPI AG in Microorganisms
- Vol. 14 (5) , 1009
Intra-Omicron Reinfection with JN.1.16 and NB.1.8.1 in a Preterm Infant: First NB.1.8.1 Detection in Tunisia—A Case Report
Highly mutated Omicron sub-lineages JN.1 and NB.1.8.1 harbor extensive spike changes, but their impact in preterm infants is poorly documented. We report a preterm male infant with three hospitalizations in seven weeks: severe SARS-CoV-2 ARDS at 40 days of life (DOL 40) requiring ventilation caused by JN.1.16, HCoV-OC43 infection at DOL 65, and a mild SARS-CoV-2 reinfection at DOL 87 due to NB.1.8.1, the first detection of this variant in Tunisia. Spike analysis showed a shared JN.1 backbone but distinct N-terminal and receptor-binding domain changes, supporting intra-Omicron reinfection driven by antigenic divergence and immature immunity and underscoring the value of pediatric genomic surveillance, including phylogenetic placement of case genomes within local Omicron diversity.
- 30 April 2026
- Published by MDPI AG in Microorganisms
- Vol. 14 (5) , 1009
Open AccessIntra-Omicron Reinfection with JN.1.16 and NB.1.8.1 in a Preterm Infant: First NB.1.8.1 Detection in Tunisia—A Case Report
Highly mutated Omicron sub-lineages JN.1 and NB.1.8.1 harbor extensive spike changes, but their impact in preterm infants is poorly documented. We report a preterm male infant with three hospitalizations in seven weeks: severe SARS-CoV-2 ARDS at 40 days of life (DOL 40) requiring ventilation caused by JN.1.16, HCoV-OC43 infection at DOL 65, and a mild SARS-CoV-2 reinfection at DOL 87 due to NB.1.8.1, the first detection of this variant in Tunisia. Spike analysis showed a shared JN.1 backbone but distinct N-terminal and receptor-binding domain changes, supporting intra-Omicron reinfection driven by antigenic divergence and immature immunity and underscoring the value of pediatric genomic surveillance, including phylogenetic placement of case genomes within local Omicron diversity.