a) There's no need for there to be an intermediary species. The "What is the probability of this pattern occuring in the case of a natural spillover? It's 1:atoms-in-the universe level" statement in the comment I replied to is just wrong - it's unusual, but nothing like as mind bogglingly impossibly rare are they claim.
b) Genetic analysis indicates that it most likely came from bats directly to humans, but picked up the ACE2 receptors from a Pangolin virus that was passed back to bats, evolved there and then infected humans. To quote the same nature article I lined above:
However, on closer inspection, the relative divergences in the phylogenetic tree (Fig. 2, bottom) show that SARS-CoV-2 is unlikely to have acquired the variable loop from an ancestor of Pangolin-2019 because these two sequences are approximately 10–15% divergent throughout the entire S protein (excluding the N-terminal domain). It is RaTG13 that is more divergent in the variable-loop region (Extended Data Fig. 1) and thus likely to be the product of recombination, acquiring a divergent variable loop from a hitherto unsampled bat sarbecovirus28. This is notable because the variable-loop region contains the six key contact residues in the RBD that give SARS-CoV-2 its ACE2-binding specificity27,37. These residues are also in the Pangolin Guangdong 2019 sequence. The most parsimonious explanation for these shared ACE2-specific residues is that they were present in the common ancestors of SARS-CoV-2, RaTG13 and Pangolin Guangdong 2019, and were lost through recombination in the lineage leading to RaTG13. This provides compelling support for the SARS-CoV-2 lineage being the consequence of a direct or nearly-direct zoonotic jump from bats, because the key ACE2-binding residues were present in viruses circulating in bats.
and:
Although the human ACE2-compatible RBD was very likely to have been present in a bat sarbecovirus lineage that ultimately led to SARS-CoV-2, this RBD sequence has hitherto been found in only a few pangolin viruses.
b) Genetic analysis indicates that it most likely came from bats directly to humans, but picked up the ACE2 receptors from a Pangolin virus that was passed back to bats, evolved there and then infected humans. To quote the same nature article I lined above:
However, on closer inspection, the relative divergences in the phylogenetic tree (Fig. 2, bottom) show that SARS-CoV-2 is unlikely to have acquired the variable loop from an ancestor of Pangolin-2019 because these two sequences are approximately 10–15% divergent throughout the entire S protein (excluding the N-terminal domain). It is RaTG13 that is more divergent in the variable-loop region (Extended Data Fig. 1) and thus likely to be the product of recombination, acquiring a divergent variable loop from a hitherto unsampled bat sarbecovirus28. This is notable because the variable-loop region contains the six key contact residues in the RBD that give SARS-CoV-2 its ACE2-binding specificity27,37. These residues are also in the Pangolin Guangdong 2019 sequence. The most parsimonious explanation for these shared ACE2-specific residues is that they were present in the common ancestors of SARS-CoV-2, RaTG13 and Pangolin Guangdong 2019, and were lost through recombination in the lineage leading to RaTG13. This provides compelling support for the SARS-CoV-2 lineage being the consequence of a direct or nearly-direct zoonotic jump from bats, because the key ACE2-binding residues were present in viruses circulating in bats.
and:
Although the human ACE2-compatible RBD was very likely to have been present in a bat sarbecovirus lineage that ultimately led to SARS-CoV-2, this RBD sequence has hitherto been found in only a few pangolin viruses.
https://www.nature.com/articles/s41564-020-0771-4