Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
The temperature dependence of infection reflects changes in performance of parasites and hosts. High temperatures often mitigate infection by favoring heat-tolerant hosts over heat-sensitive parasites. Honey bees exhibit endothermic thermoregulation-rare among insects-that can favor resistance to parasites. However, viruses are heavily host-dependent, suggesting that viral infection could be supported-not threatened-by optimum host function. To understand how temperature-driven changes in performance of viruses and hosts shape infection, we compared the temperature dependence of isolated viral enzyme activity, three honey bee traits, and infection of honey bee pupae. Viral enzyme activity varied <2-fold over a > 30 °C interval spanning temperatures typical of ectothermic insects and honey bees. In contrast, honey bee performance peaked at high (≥ 35 °C) temperatures and was highly temperature-sensitive. Although these results suggested that increasing temperature would favor hosts over viruses, the temperature dependence of pupal infection matched that of pupal development, falling only near pupae's upper thermal limits. Our results reflect the host-dependent nature of viruses, suggesting that infection is accelerated-not curtailed-by optimum host function, contradicting predictions based on relative performance of parasites and hosts, and suggesting tradeoffs between infection resistance and host survival that limit the viability of bee 'fever'.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10042853 | PMC |
http://dx.doi.org/10.1038/s42003-023-04704-6 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!