The research addresses a novel and intriguing hypothesis regarding the parasite's capacity to respond to mosquito bites, and whether such responses are specific to competent vectors or generalized to any mosquito species. This is an important and timely question. The authors provide a valuable contribution to the field of parasite-vector-host interactions. The use of the avian malaria system is well-justified, offering a tractable and ecologically relevant model where parasites are not under intense selective pressure, as is often the case in human malaria systems. The manuscript is well-written, and the methodology is overall appropriate for the study objectives.
Several points require clarification or elaboration. Below are specific comments for consideration.

Please clarify whether the infectious dose was standardized across individuals. Variation in the number of inoculated meronts could have influenced gametocyte production and other downstream variables.

Could authors specify the origin of the parasite isolate used? From which bird species was the SGS1 lineage originally obtained? Were all recipient birds infected with the same isolate to ensure comparability?

Some methodological choices could be better explained. Please clarify whether the one-month period post-infection was sufficient to reliably establish chronic infection across all individuals. Additionally, provide details on how parasitemia was monitored before mosquito exposure. Finally, justify the selection of specific blood sampling days (D0, D1–D3, D4, D7) and explain the biological or experimental rationale behind this timeline.

The sampling strategy for assessing host physiological responses is unclear. The authors state that to determine whether bites from mosquitoes elicit distinct host physiological responses, birds were exposed to mosquitoes over three consecutive days under the same experimental conditions as described earlier in the text. Please clarify how many birds were used per group, how much blood was collected per individual, and on which exact days blood sampling occurred.

Corticosterone levels can fluctuate rapidly in response to stress, often within minutes. Therefore, detailed information about the handling protocols, time between capture and sampling, and any measures taken to reduce handling-induced stress is essential for interpreting these data.

Line 153: The text currently refers to a figure incorrectly. It should likely read Figure S1.

The discussion on the lack of short-term plasticity in P. relictum’s gametocyte traits is compelling, particularly in contrast with P. falciparum and P. chabaudi. However, I wonder if there would be any other possible explanations beyond developmental synchrony. For instance, could differences in host erythrocyte lifespan or parasite tropism for different erythrocyte types also influence transmission investment strategies?

The manuscript is clearly written, the experimental methods are sound, and the conclusions are generally well-supported by the data. Addressing the points above would further strengthen the manuscript and its contribution to our understanding of malaria parasite transmission strategies.