About this Research Topic
In immunocompromised populations like diabetics, burn victims, HIV patients, organ transplant recipients, etc., superbugs, increase morbidity. Investigating transmission mechanisms and pathways is difficult. Genomic markers can identify an infection's genesis but not necessarily its dissemination. Control strategy, disease spread, and epidemiological results differ due to many transmission routes.
Recent genotyping methods enable genome-wide natural selection searches. Identifying natural selection targets can improve human adaptation and evolution research and help determine which variants affect normal human phenotypic variation and sickness vulnerability. Population genomics idea has helped us grasp new evolution concerns by providing new perspectives.
Density-dependent fertility limits seem to drive long-term stability, while habitat type drives population abundance. Abundance may cycle in moderate-to-poor settings. The social organization and behavior of host species, the lengthy infectiousness of sick animals, the presence of carriers and inactive cases, and disease stability appear to be related. Phages can exert evolutionary pressure on bacterial populations by altering their DNA to make them more resistant to infection. Phage-binding receptors, superinfection exclusion, CRISPR-Cas, and restriction-modification systems mediate phage-bacterial interactions.
In this collection, we will accept papers with details on:
1. How superbugs increase morbidity in vulnerable populations like diabetics, burn victims, HIV patients, and organ transplant recipients.
2. Molecular epidemiology of disease transmission (mode and route), diversity of Control tactics, and disease spread.
3. Metagenomics of Host-pathogen interactions involving multiple transmission mechanisms, routes, origin, and dissemination profiles.
4. Identification of natural selection targets to improve human adaptation, sickness vulnerability, and evolution research profiles.
5. Use of Genome-wide and OMICS technologies, cutting-edge sequencing, bioinformatics, and statistics to highlight evolutionary and population genetics, population size, demographic history, structure phenotypes, and local adaptation.
6. Modeling and evaluating superbug-related disease geographic spread to show how transmission varies with distance.
7. The role of density-dependent fertility limits, as a driver of long-term stability and habitat type as a driver of population abundance.
8. The inter-relatedness of social organization and behavior of host species, the lengthy infectiousness of sick host, the presence of carriers and inactive cases.
9. The role of Phages in exerting evolutionary pressure on bacterial populations: alteration of DNA, phage target sites, outer membranes, and replication inhibitors
10. Papers that shed light on phage-bacterial interactions such as Phage-binding receptors, superinfection exclusion, CRISPR-Cas, and restriction-modification systems
The list of superbugs under consideration includes:
1. Acinetobacter baumannii (carbapenem resistant),
2. Pseudomonas aeruginosa (carbapenem resistant),
3. Enterobacteriaceae (carbapenem resistant),
4. Extended‐spectrum beta-lactamases-producing bacteria
5. Neisseria gonorrhoeae (cephalosporin and fluoroquinolone-resistant),
6. Enterococcus faecium (vancomycin-resistant),
7. nontyphoidal Salmonella (fluoroquinolones resistant),
8. Staphylococcus aureus (methicillin and vancomycin-resistant),
9. Helicobacter pylori (clarithromycin resistant), and
10. Campylobacter spp. (fluoroquinolone resistant);
11. Haemophilus influenzae (ampicillin resistant),
12. Shigella species (fluoroquinolones resistant)
13. Streptococcus pneumoniae (penicillin-resistant)
14. Klebsiella pneumoniae (carbapenems and cephalosporin resistant),
15. Escherichia coli (fluoroquinolones and cephalosporin-resistant),
16. Mycobacterium tuberculosis (fluoroquinolone, rifampicin, and isoniazid resistant),
17. Aspergillus spp.,
18. Candida auris and non albican strains
19. Leishmania,
20. Plasmodia
Recent genotyping methods enable genome-wide natural selection searches. Identifying natural selection targets can improve human adaptation and evolution research and help determine which variants affect normal human phenotypic variation and sickness vulnerability. Population genomics idea has helped us grasp new evolution concerns by providing new perspectives.
Density-dependent fertility limits seem to drive long-term stability, while habitat type drives population abundance. Abundance may cycle in moderate-to-poor settings. The social organization and behavior of host species, the lengthy infectiousness of sick animals, the presence of carriers and inactive cases, and disease stability appear to be related. Phages can exert evolutionary pressure on bacterial populations by altering their DNA to make them more resistant to infection. Phage-binding receptors, superinfection exclusion, CRISPR-Cas, and restriction-modification systems mediate phage-bacterial interactions.
In this collection, we will accept papers with details on:
1. How superbugs increase morbidity in vulnerable populations like diabetics, burn victims, HIV patients, and organ transplant recipients.
2. Molecular epidemiology of disease transmission (mode and route), diversity of Control tactics, and disease spread.
3. Metagenomics of Host-pathogen interactions involving multiple transmission mechanisms, routes, origin, and dissemination profiles.
4. Identification of natural selection targets to improve human adaptation, sickness vulnerability, and evolution research profiles.
5. Use of Genome-wide and OMICS technologies, cutting-edge sequencing, bioinformatics, and statistics to highlight evolutionary and population genetics, population size, demographic history, structure phenotypes, and local adaptation.
6. Modeling and evaluating superbug-related disease geographic spread to show how transmission varies with distance.
7. The role of density-dependent fertility limits, as a driver of long-term stability and habitat type as a driver of population abundance.
8. The inter-relatedness of social organization and behavior of host species, the lengthy infectiousness of sick host, the presence of carriers and inactive cases.
9. The role of Phages in exerting evolutionary pressure on bacterial populations: alteration of DNA, phage target sites, outer membranes, and replication inhibitors
10. Papers that shed light on phage-bacterial interactions such as Phage-binding receptors, superinfection exclusion, CRISPR-Cas, and restriction-modification systems
The list of superbugs under consideration includes:
1. Acinetobacter baumannii (carbapenem resistant),
2. Pseudomonas aeruginosa (carbapenem resistant),
3. Enterobacteriaceae (carbapenem resistant),
4. Extended‐spectrum beta-lactamases-producing bacteria
5. Neisseria gonorrhoeae (cephalosporin and fluoroquinolone-resistant),
6. Enterococcus faecium (vancomycin-resistant),
7. nontyphoidal Salmonella (fluoroquinolones resistant),
8. Staphylococcus aureus (methicillin and vancomycin-resistant),
9. Helicobacter pylori (clarithromycin resistant), and
10. Campylobacter spp. (fluoroquinolone resistant);
11. Haemophilus influenzae (ampicillin resistant),
12. Shigella species (fluoroquinolones resistant)
13. Streptococcus pneumoniae (penicillin-resistant)
14. Klebsiella pneumoniae (carbapenems and cephalosporin resistant),
15. Escherichia coli (fluoroquinolones and cephalosporin-resistant),
16. Mycobacterium tuberculosis (fluoroquinolone, rifampicin, and isoniazid resistant),
17. Aspergillus spp.,
18. Candida auris and non albican strains
19. Leishmania,
20. Plasmodia
Keywords: superbugs, epidemiology, transmission, metagenomics, OMICS, bioinformatics, disease transmission, phages, CRISPR-Cas, HIV
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